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| 0.9977 | Methylation | CheY - dependent Methylationmethylation of the asparagine receptor, ProteinMcpB , during chemotaxis in Bacillus subtilis. |
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| 0.9996 | Methylation | In this study, we show that rapid net Methylationdemethylation of B. subtilis ProteinMcpB results in the immediate production of methanol, presumably due to the action of CheB. |
| Methylation | In this study, we show that rapid net Demethylationdemethylation of B. subtilis ProteinMcpB results in the immediate production of methanol, presumably due to the action of CheB. | |
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| 1.0000 | Methylation | We also show that net Methylationdemethylation of ProteinMcpB occurs upon both addition and removal of asparagine. |
| Methylation | We also show that net Demethylationdemethylation of ProteinMcpB occurs upon both addition and removal of asparagine. | |
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| 1.0000 | Methylation | After each demethylation event, ProteinMcpB is Methylationremethylated to nearly prestimulus levels. |
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| 1.0000 | Methylation | Both Methylationremethylation events are attributable to ProteinCheR using S - adenosylmethionine as a substrate. |
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| 0.9997 | Methylation | Furthermore, we show that the Methylationremethylation of asparagine - bound ProteinMcpB requires the response regulator, CheY - P, suggesting that CheY - P acts in a feedback mechanism to facilitate adaptation to positive stimuli during chemotaxis in B. subtilis. |
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| 0.9999 | Methylation | Effect of alternative Glycosylationglycosylation on Proteininsulin receptor processing. |
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| 1.0000 | Methylation | To examine the importance of GlycosylationN - linked glycosylation on Proteininsulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 1.0000 | Methylation | To examine the importance of N - linked Glycosylationglycosylation on Proteininsulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 0.9868 | Methylation | To examine the importance of GlycosylationN - linked glycosylation on Proteininsulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 0.8955 | Methylation | To examine the importance of GlycosylationN - linked glycosylation Glycosylationglycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 0.8526 | Methylation | To examine the importance of GlycosylationN - linked glycosylation Glycosylationglycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 0.7830 | Methylation | To examine the importance of GlycosylationN - linked GlycosylationN - linked glycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 0.7803 | Methylation | To examine the importance of GlycosylationN - linked Glycosylationglycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 0.7278 | Methylation | To examine the importance of GlycosylationN - linked Glycosylationglycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
| 0.6470 | Methylation | To examine the importance of GlycosylationN - linked glycosylation GlycosylationN - linked glycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation. |
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| 0.9957 | Methylation | N - Glycosidase F treatment shows that the alternative proreceptor contained GlycosylationN - linked Entityoligosaccharides . |
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| 0.9999 | Methylation | OBJECTIVES : To develop an enzyme - linked immunosorbent assay ( ELISA ) using a monoclonal antibody ( mab ) directed against abnormally Glycosylationglycosylated serum Proteinalpha2 - macroglobulin ( alpha2 - M ) from patients with systemic lupus erythematosus ( SLE ). |
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| 1.0000 | Methylation | CONCLUSIONS : The ELISA was capable of recognizing changes of Glycosylationglycosylation of Proteinalpha2 - M in SLE and may be useful for its differential diagnosis. |
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| 0.9980 | Methylation | We investigated the kinetics of mRNA induction, demethylation, and DNA_methylationremethylation of the p16 Entitypromoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.9950 | Methylation | We investigated the kinetics of mRNA induction, demethylation, and DNA_methylationremethylation of the p16 promoter and Entitysecond - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.9788 | Methylation | We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between EntityCpG island DNA_methylationmethylation and gene transcription. |
| 0.9943 | Methylation | We investigated the kinetics of mRNA induction, DNA_methylationdemethylation , and remethylation of the p16 Entitypromoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.9931 | Methylation | We investigated the kinetics of mRNA induction, DNA_methylationdemethylation , and remethylation of the p16 promoter and Entitysecond - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.9921 | Methylation | We investigated the kinetics of mRNA induction, demethylation, and DNA_methylationremethylation of the p16 promoter and second - exon EntityCpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| 0.9882 | Methylation | We investigated the kinetics of mRNA induction, DNA_methylationdemethylation , and remethylation of the p16 promoter and second - exon EntityCpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. |
| Methylation | We investigated the kinetics of mRNA induction, DNA_demethylationdemethylation , and remethylation of the p16 promoter and Entitysecond - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. | |
| Methylation | We investigated the kinetics of mRNA induction, DNA_demethylationdemethylation , and remethylation of the p16 Entitypromoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription. | |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9988 | Methylation | The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and DNA_methylationremethylation of the p16 Entityexon 2 CpG island occurred at a higher rate than that of the p16 promoter. |
| 0.9892 | Methylation | The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and DNA_methylationremethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the p16 Entitypromoter . |
| 0.9999 | Methylation | The rates of DNA_methylationremethylation of both EntityCpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the p16 promoter. |
| 0.9935 | Methylation | The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and DNA_methylationremethylation of the p16 exon 2 EntityCpG island occurred at a higher rate than that of the p16 promoter. |
| 0.4095 | Methylation | The rates of DNA_methylationremethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 Entityexon 2 CpG island occurred at a higher rate than that of the p16 promoter. |
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| 0.9991 | Methylation | The kinetics of DNA_methylationremethylation of the p16 Entityexon 2 , PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9985 | Methylation | The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 Entityexon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are DNA_methylationhypermethylated in T24 cells. |
| 0.9966 | Methylation | The kinetics of remethylation of the p16 exon 2, PAX - 6 Entityexon 5 , c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are DNA_methylationhypermethylated in T24 cells. |
| 0.9964 | Methylation | The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL Entityexon 11 , and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are DNA_methylationhypermethylated in T24 cells. |
| 0.9959 | Methylation | The kinetics of DNA_methylationremethylation of the p16 exon 2, PAX - 6 Entityexon 5 , c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9953 | Methylation | The kinetics of DNA_methylationremethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 Entityexon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9943 | Methylation | The kinetics of DNA_methylationremethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL Entityexon 11 , and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9932 | Methylation | The kinetics of remethylation of the p16 Entityexon 2 , PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are DNA_methylationhypermethylated in T24 cells. |
| 0.9966 | Methylation | The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 Entityexon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are DNA_methylationhypermethylated in T24 cells. |
| 0.9911 | Methylation | The kinetics of DNA_methylationremethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 Entityexon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| 0.9892 | Methylation | The kinetics of remethylation of the p16 exon 2, PAX - 6 Entityexon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are DNA_methylationhypermethylated in T24 cells. |
| 0.9873 | Methylation | The kinetics of DNA_methylationremethylation of the p16 exon 2, PAX - 6 Entityexon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. |
| Score | Relation | Text (Head - Tail) |
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| 0.9997 | Methylation | DNA_methylationRemethylation occurred most rapidly in the p16, ProteinPAX - 6 , and c - ABL genes, shown to be transcribed prior to drug treatment. |
| 0.9996 | Methylation | DNA_methylationRemethylation occurred most rapidly in the Proteinp16 , PAX - 6, and c - ABL genes, shown to be transcribed prior to drug treatment. |
| 0.9994 | Methylation | DNA_methylationRemethylation occurred most rapidly in the p16, PAX - 6, and Proteinc - ABL genes, shown to be transcribed prior to drug treatment. |
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| 0.9997 | Methylation | Also, marked relationship of microsatellite instability ( MSI ) and DNA methylation has been reported in sporadic colorectal cancer, which is a result of epigenetic inactivation of hMLH1 in association of Entitypromoter DNA_methylationhypermethylation . |
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| 0.9990 | Methylation | In the present study, we investigated the Entity5'CpG island DNA_methylationhypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| 0.9993 | Methylation | In the present study, we investigated the 5 ' EntityCpG island DNA_methylationhypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| 0.8317 | Methylation | In the present study, we investigated the 5 ' EntityCpG island DNA_methylationhypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
| 0.7899 | Methylation | In the present study, we investigated the Entity5'CpG island DNA_methylationhypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status. |
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| 0.9982 | Methylation | Of the 8 MSI - H patients, 5 presented hMLH1 methylation, whereas no low - frequency MSI ( MSI - L ) and microsatellite stable ( MSS ) cases exhibited ProteinhMLH1 DNA_methylationmethylation ( 5 / 8 vs. 0 / 43, p < 0. 00001 ). |
| 0.9978 | Methylation | Of the 8 MSI - H patients, 5 presented ProteinhMLH1 DNA_methylationmethylation , whereas no low - frequency MSI ( MSI - L ) and microsatellite stable ( MSS ) cases exhibited hMLH1 methylation ( 5 / 8 vs. 0 / 43, p < 0. 00001 ). |
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| 0.9997 | Methylation | Furthermore, these patients also presented ProteinE - cadherin and p16 DNA_methylationhypermethylation . |
| 0.9979 | Methylation | Furthermore, these patients also presented E - cadherin and Proteinp16 DNA_methylationhypermethylation . |
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| 0.9984 | Methylation | Our data showed a significant correlation between ProteinhMLH1 DNA_methylationmethylation and MSI in GC, and suggested that a common mechanism of aberrant de novo methylation can be postulated in these cancers. |
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| 1.0000 | Methylation | However, only Glycosylationglycosylated proteins Protein( TSHR - hs and TSHR - gp ) neutralized the TBII activity of sera from autoimmune thyroid patients, confirming the importance of glycosylation for patient autoantibody reactivity. |
| 0.9998 | Methylation | However, only Glycosylationglycosylated proteins ( TSHR - hs and ProteinTSHR - gp ) neutralized the TBII activity of sera from autoimmune thyroid patients, confirming the importance of glycosylation for patient autoantibody reactivity. |
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| 1.0000 | Methylation | BasT - inactivated mutant cells are missing a membrane protein radiolabelled with L - [ methyl - 3H ] - methionine in wild - type cells, confirming that ProteinBasT is Methylationmethylatable and membrane bound. |
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| 1.0000 | Methylation | Additional GlycosylationN - glycosylation at EntityAsn ( 13 ) rescues the human LHbeta - subunit from disulfide - linked aggregation. |
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| 1.0000 | Methylation | Both CGbeta wild - type ( WT ) and CGbeta lacking GlycosylationN - glycosylation at EntityAsn ( 13 ) ( CGbeta - N13 ) showed aggregates in lysate. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 1.0000 | Methylation | These results indicate that the backbone structure consisting of 114 amino acids and GlycosylationN - linked glycosylation at EntityAsn ( 30 ) is involved in the aggregation of LHbeta. |
| 1.0000 | Methylation | These results indicate that the backbone structure consisting of 114 amino acids and N - linked Glycosylationglycosylation at EntityAsn ( 30 ) is involved in the aggregation of LHbeta. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 1.0000 | Methylation | Moreover, GlycosylationN - glycosylation at EntityAsn ( 13 ) does not prevent such aggregation, but instead plays an important role in correct folding for both LHbeta - and CGbeta - subunits to be secreted as monomer. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
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| 0.9999 | Methylation | Type XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and Hydroxylationhydroxylation of Entityproline residues dramatically enhanced this association. |
| 0.9997 | Methylation | Type XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and Hydroxylationhydroxylation of Entityproline residues dramatically enhanced this association. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
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| 0.9970 | Methylation | Symmetric and asymmetric DNA_methylationDNA methylation in the human IGF2 - H19 Entityimprinted region . |
| 0.9973 | Methylation | Symmetric and asymmetric DNA DNA_methylationmethylation in the human IGF2 - H19 Entityimprinted region . |
| 0.9923 | Methylation | Symmetric and asymmetric DNA DNA_methylationmethylation in the human IGF2 - H19 Entityimprinted region. |
| 0.9913 | Methylation | Symmetric and asymmetric DNA_methylationDNA methylation in the human IGF2 - H19 Entityimprinted region. |
| 0.9487 | Methylation | Symmetric and asymmetric DNA_methylationDNA methylation in the human IGF2 - H19 Entityimprinted region . |
| 0.8638 | Methylation | Symmetric and asymmetric DNA_methylationDNA methylation in the human IGF2 - H19 Entityimprinted region. |
| 0.6757 | Methylation | Symmetric and asymmetric DNA_methylationDNA DNA_methylationmethylation in the human IGF2 - H19 imprinted region. |
| 0.6489 | Methylation | Symmetric and asymmetric DNA_methylationDNA DNA_methylationDNA methylation in the human IGF2 - H19 imprinted region. |
| 0.6317 | Methylation | Symmetric and asymmetric DNA_methylationDNA methylation DNA_methylationmethylation in the human IGF2 - H19 imprinted region. |
| 0.5755 | Methylation | Symmetric and asymmetric DNA_methylationDNA methylation DNA_methylationmethylation in the human IGF2 - H19 imprinted region. |
| 0.4911 | Methylation | Symmetric and asymmetric DNA_methylationDNA methylation DNA_methylationDNA methylation in the human IGF2 - H19 imprinted region. |
| 0.4623 | Methylation | Symmetric and asymmetric DNA_methylationDNA DNA_methylationmethylation in the human IGF2 - H19 imprinted region. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| Score | Relation | Text (Head - Tail) |
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| 0.9981 | Methylation | The presence of a differential DNA_methylationmethylation region ( DMR ) on the two parental alleles at the Entity5'flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.9980 | Methylation | The presence of a differential DNA_methylationmethylation region ( DMR ) on the two parental alleles at the Entity5'flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.9970 | Methylation | The presence of a differential DNA_methylationmethylation region ( DMR ) on the two parental alleles at the Entity5 ' flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.9970 | Methylation | The presence of a differential DNA_methylationmethylation region ( DMR ) on the two parental alleles at the 5 ' Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.9968 | Methylation | The presence of a differential DNA_methylationmethylation region ( DMR ) on the two parental alleles at the 5 ' Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.5844 | Methylation | The presence of a differential methylation region ( DMR ) on the two parental alleles at the 5 ' Entityflanking Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.5536 | Methylation | The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5'flanking region Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.5433 | Methylation | The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5'flanking Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.4431 | Methylation | The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5 ' Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.4217 | Methylation | The presence of a differential methylation region ( DMR ) on the two parental alleles at the 5 ' Entityflanking region Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.4042 | Methylation | The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5'flanking region Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| 0.4023 | Methylation | The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5'flanking region Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9997 | Methylation | Using bisulfite genomic sequencing, we have assessed the DNA_methylationmethylation status of Entitycytosine ( including 154 CpG sites ) in six CpG - rich regions of the human IGF2 - H19 genes. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9999 | Methylation | In a CpG island near promoter P3 of the IGF2 gene, more than 99. 8 % of all cytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the EntityCpGs was DNA_methylationmethylated . |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9999 | Methylation | In the IGF2 exon 8 - 9 region, mosaic DNA_methylationmethylation of 56 EntityCpG sites was observed in fetal tissues and in adult blood DNA. |
| 0.9997 | Methylation | In the IGF2 exon 8 - 9 region, mosaic DNA_methylationmethylation of 56 EntityCpG sites was observed in fetal tissues and in adult blood DNA. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9999 | Methylation | In contrast to the mosaic DNA_methylationmethylation of ProteinIGF2 , the allelic methylation of the human H19 DMR was uniform. |
| 0.9959 | Methylation | In contrast to the mosaic methylation of IGF2, the allelic DNA_methylationmethylation of the human H19 EntityDMR was uniform. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 1.0000 | Methylation | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all Entity25 CpG sites were completely DNA_methylationmethylated on only one parental allele. |
| 1.0000 | Methylation | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all 25 EntityCpG sites were completely DNA_methylationmethylated on only one parental allele. |
| 0.9982 | Methylation | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all Entity25 CpG sites were completely DNA_methylationmethylated on only one parental allele. |
| 0.9975 | Methylation | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all Entity25 CpG sites were completely DNA_methylationmethylated on only one parental allele. |
| 0.9974 | Methylation | In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all 25 EntityCpG sites were completely DNA_methylationmethylated on only one parental allele. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9999 | Methylation | Uniform allele - specific DNA_methylationmethylation was also observed in the EntityCpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete methylation of all 25 CpG sites in one parental allele. |
| 0.9999 | Methylation | Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete DNA_methylationmethylation of all 25 EntityCpG sites in one parental allele. |
| 0.9999 | Methylation | Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with DNA_methylationcomplete methylation of all 25 EntityCpG sites in one parental allele. |
| Methylation | Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete DNA_methylationmethylation of all Entity25 CpG sites in one parental allele. | |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9989 | Methylation | In contrast, the EntityCpG region in the H19 promoter ( - 292 to + 15 ) was mosaically DNA_methylationmethylated in all tissues. |
| 0.9930 | Methylation | In contrast, the EntityCpG region in the H19 promoter ( - 292 to + 15 ) was mosaically DNA_methylationmethylated in all tissues. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 1.0000 | Methylation | In addition, cytosine was DNA_methylationmethylated at three EntityCpNpG and GpNpC sites on the top DNA strand and one CpNpG site on the bottom DNA strand from the fetal brain. |
| 0.9997 | Methylation | In addition, cytosine was DNA_methylationmethylated at three CpNpG and EntityGpNpC sites on the top DNA strand and one CpNpG site on the bottom DNA strand from the fetal brain. |
| 0.9988 | Methylation | In addition, cytosine was DNA_methylationmethylated at three CpNpG and GpNpC sites on the top DNA strand and one EntityCpNpG site on the bottom DNA strand from the fetal brain. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9987 | Methylation | The cytosines at CpG sites were methylated on both DNA strands ( symmetric methylation ) while Entitycytosines at the CpNpG and GpNpC sites were DNA_methylationmethylated on only one DNA strand ( asymmetric methylation ). |
| 0.9955 | Methylation | The Entitycytosines at CpG sites were DNA_methylationmethylated on both DNA strands ( symmetric methylation ) while cytosines at the CpNpG and GpNpC sites were methylated on only one DNA strand ( asymmetric methylation ). |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9992 | Methylation | The asymmetric DNA_methylationmethylation was associated with tissue - specific disruption of ProteinH19 genomic imprinting in fetal brain. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9985 | Methylation | An increase in Proteinhistone Acetylationacetylation and IL - 2 antagonizing the immunoinhibitory effect are necessary for augmentation by butyrate of in vitro anti - TNP antibody production. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9997 | Methylation | We investigated the role of Proteinhistone Acetylationacetylation in the promotion of antigen - specific antibody production in murine B cells induced by sodium butyrate ( NaBu ) plus interleukin 2 ( IL - 2 ). |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9999 | Methylation | NaBu dose dependently increased the Acetylationacetylation levels of Proteinhistone H4 at concentrations which effectively enhanced anti - trinitrophenyl ( TNP ) antibody production in the presence of IL - 2. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9980 | Methylation | Among other short - chain fatty acids and NaBu analogs, propionate, valerate and vinylacetate were effective in the presence of IL - 2 in increasing both antibody production and the Proteinhistone H4 Acetylationacetylation level, but acetate, alpha -, beta - and gamma - hydroxybutyrates and alpha -, beta - and gamma - aminobutyrates were not effective, even in the presence of IL - 2. |
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| 1.0000 | Methylation | Splenic B cells treated with NaBu, TSA and both together in the presence or absence of IL - 2 showed almost the same increased Acetylationacetylation level of Proteinhistone H4 . |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9989 | Methylation | These results suggest that the NaBu - induced enhancement of anti - TNP antibody production in the presence of IL - 2 is mediated through a moderate increase in the level of Proteinhistone Acetylationacetylation and that NaBu has both stimulating and inhibiting activities for anti - TNP antibody production, the latter of which is overcome by IL - 2. |
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| 0.9994 | Methylation | Evidence that the lizard Proteinhelospectin peptides are GlycosylationO - glycosylated . |
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| 0.9980 | Methylation | The Glycosylationglycosylation did not affect the capacity of the Proteinhelospectins to recognize and to activate the human and the rat VPAC1 and VPAC2 receptors. |
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| 1.0000 | Methylation | Hepatic levels of methionine, SAM, and DNA methylation fell by approximately 40 %. Proteinc - myc was DNA_methylationhypomethylated , and its mRNA level increased. |
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| 1.0000 | Methylation | Calf histones H2A and H4 and bovine Proteinmyelin basic protein were Catalysismethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. |
| 1.0000 | Methylation | Calf histones H2A and H4 and bovine myelin basic protein were Catalysismethylated by ProteinHsl7p , whereas histones H1, H2B, and H3 and bovine cytochrome c were not. |
| 0.9997 | Methylation | Calf histones H2A and H4 and bovine myelin basic protein were Catalysismethylated by Hsl7p, whereas histones H1, ProteinH2B , and H3 and bovine cytochrome c were not. |
| 0.9997 | Methylation | Calf histones H2A and H4 and bovine myelin basic protein were Catalysismethylated by Hsl7p, whereas Proteinhistones H1 , H2B, and H3 and bovine cytochrome c were not. |
| 0.9995 | Methylation | Calf histones H2A and H4 and bovine myelin basic protein were Catalysismethylated by Hsl7p, whereas histones H1, H2B, and ProteinH3 and bovine cytochrome c were not. |
| 0.9993 | Methylation | Calf histones H2A and ProteinH4 and bovine myelin basic protein were Catalysismethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. |
| 0.9992 | Methylation | Calf histones H2A and H4 and bovine myelin basic protein were Catalysismethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine Proteincytochrome c were not. |
| 0.9974 | Methylation | Calf Proteinhistones H2A and H4 and bovine myelin basic protein were Catalysismethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. |
| Methylation | Calf histones H2A and H4 and bovine myelin basic protein were Methylationmethylated by Hsl7p, whereas histones H1, ProteinH2B , and H3 and bovine cytochrome c were not. | |
| Methylation | Calf histones H2A and H4 and bovine myelin basic protein were Methylationmethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine Proteincytochrome c were not. | |
| Methylation | Calf histones H2A and H4 and bovine myelin basic protein were Methylationmethylated by Hsl7p, whereas Proteinhistones H1 , H2B, and H3 and bovine cytochrome c were not. | |
| Methylation | Calf Proteinhistones H2A and H4 and bovine myelin basic protein were Methylationmethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. | |
| Methylation | Calf histones H2A and H4 and bovine myelin basic protein were Methylationmethylated by ProteinHsl7p , whereas histones H1, H2B, and H3 and bovine cytochrome c were not. | |
| Methylation | Calf histones H2A and H4 and bovine myelin basic protein were Methylationmethylated by Hsl7p, whereas histones H1, H2B, and ProteinH3 and bovine cytochrome c were not. | |
| Methylation | Calf histones H2A and H4 and bovine Proteinmyelin basic protein were Methylationmethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. | |
| Methylation | Calf histones H2A and ProteinH4 and bovine myelin basic protein were Methylationmethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not. | |
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| 0.9998 | Methylation | Rapid induction of Proteinhistone Acetylationhyperacetylation and cellular differentiation in human breast tumor cell lines following degradation of histone deacetylase - 1. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
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| 0.9985 | Methylation | AcetylationHyperacetylated Proteinhistone H4 appeared within 2 h of the addition of quinidine to the medium, and levels were maximal by 24 h. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9999 | Methylation | Quinidine - treated MCF - 7 cells showed elevated Proteinp21 ( WAF1 ) , Phosphorylationhypophosphorylation and suppression of retinoblastoma protein, and down - regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin. |
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| 0.9921 | Methylation | Thus, Entityoligosaccharides Glycosylationattached to the minK subunit affect not only the gating properties, but also the pH sensitivity of I ( sK ). |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 1.0000 | Methylation | A novel post - translational modification of yeast elongation factor 1A. MethylationMethylesterification at the C Entityterminus . |
| 1.0000 | Methylation | A novel post - translational modification of yeast elongation factor 1A. MethylationMethylesterification at the C Entityterminus. |
| 0.9999 | Methylation | A novel post - translational modification of yeast elongation factor 1A. MethylationMethylesterification at the C terminus Entity. |
| Methylation | A novel post - translational modification of yeast elongation factor 1A. Methylesterification Methylationat the C Entityterminus. | |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
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| 0.9999 | Methylation | Previous studies have shown that eEF1A is Methylationmethylated on several internal Entitylysine residues to give mono -, di -, and tri - N - epsilon - methyl - lysine derivatives. |
| 0.9996 | Methylation | Previous studies have shown that eEF1A is Methylationmethylated on several internal Entitylysine residues to give mono -, di -, and tri - N - epsilon - methyl - lysine derivatives. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9999 | Methylation | In cycloheximide - treated cells, Methylationmethyl esterified ProteineEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction. |
| 0.9992 | Methylation | In cycloheximide - treated cells, methyl esterified ProteineEF1A was detected largely in the ribosome and polysome fractions ; little or no Methylationmethylated protein was found in the soluble fraction. |
| 0.9999 | Methylation | In cycloheximide - treated cells, methyl Methylationesterified ProteineEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction. |
| 0.9999 | Methylation | In cycloheximide - treated cells, Methylationmethyl esterified ProteineEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
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|---|---|---|
| 0.9979 | Methylation | From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the MethylationN - methylated Entitylysine residues of eEF1A are stable over 4 h, whereas the eEF1A carboxyl methyl ester has a half - life of less than 10 min. |
| 0.9982 | Methylation | From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the MethylationN - methylated Entitylysine residues of eEF1A are stable over 4 h, whereas the eEF1A carboxyl methyl ester has a half - life of less than 10 min. |
| Score | Relation | Text (Head - Tail) |
|---|---|---|
| 0.9987 | Methylation | The rapid turnover of the methyl ester suggests that the Methylationmethylation / demethylation of eEF1A at the EntityC - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast. |
| 0.9988 | Methylation | The rapid turnover of the methyl ester suggests that the Methylationmethylation / demethylation of eEF1A at the EntityC - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast. |
| 0.9987 | Methylation | The rapid turnover of the methyl ester suggests that the Methylationmethylation / demethylation of eEF1A at the EntityC - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast. |
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| 0.9999 | Methylation | Post - translational Hydroxylationhydroxylation at the EntityN - terminus of the prion protein reveals presence of PPII structure in vivo. |
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| 0.9998 | Methylation | Almost complete Hydroxylationconversion of proline to 4 - hydroxyproline occurs specifically at residue EntityPro44 of this murine protein ; the same hydroxylated residue was detected, at lower levels, in PrP ( Sc ) from the brains of scrapie - infected mice. |
| 0.9960 | Methylation | Almost complete conversion of proline to 4 - hydroxyproline occurs specifically at residue EntityPro44 of this murine protein ; the same Hydroxylationhydroxylated residue was detected, at lower levels, in PrP ( Sc ) from the brains of scrapie - infected mice. |
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| 0.9999 | Methylation | Cation binding and / or post - translational Hydroxylationhydroxylation of this region of ProteinPrP may regulate its role in the physiology and pathobiology of the cell. |
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| 0.9751 | Methylation | Furthermore, loss of DNA_methylationmethylation also greatly reduced the association of another yeast B - type subunit, ProteinRts1p . |
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| 1.0000 | Methylation | Thus, Methylationmethylation of ProteinPph21p is important for formation of PP2A trimeric and dimeric complexes, and consequently, for PP2A function. |
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| 0.9991 | Methylation | E - cadherin expression is silenced by Entity5'CpG island DNA_methylationmethylation in acute leukemia. |
| 0.9994 | Methylation | E - cadherin expression is silenced by 5 ' EntityCpG island DNA_methylationmethylation in acute leukemia. |
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| 0.9982 | Methylation | In this study, we used a nested - PCR approach to examine the DNA_methylationmethylation status of the E - cadherin Entity5'CpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia. |
| 0.9988 | Methylation | In this study, we used a nested - PCR approach to examine the DNA_methylationmethylation status of the E - cadherin 5 ' EntityCpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia. |
| 0.9984 | Methylation | In this study, we used a nested - PCR approach to examine the DNA_methylationmethylation status of the E - cadherin 5 ' EntityCpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia. |
| 0.9968 | Methylation | In this study, we used a nested - PCR approach to examine the DNA_methylationmethylation status of the E - cadherin Entity5'CpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia. |
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| 1.0000 | Methylation | In normal peripheral blood mononuclear cells and bone marrow, ProteinE - cadherin was completely DNA_methylationunmethylated . |
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| 0.9999 | Methylation | In contrast, ProteinE - cadherin was aberrantly DNA_methylationmethylated in 4 of 4 ( 100 % ) leukemia cell lines, 14 of 44 ( 32 % ) acute myelogenous leukemias, and 18 of 33 ( 53 % ) acute lymphoblastic leukemias. |
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| 1.0000 | Methylation | Genomic bisulfite sequencing of primary leukemias confirmed dense DNA_methylationmethylation across the EntityCpG island . |
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| 1.0000 | Methylation | DNA_methylationMethylation was associated with loss of ProteinE - cadherin RNA and protein in leukemia cell lines and primary leukemias. |
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| 0.9997 | Methylation | Following treatment with 5 - aza - 2'- deoxycytidine, a DNA_methylationmethylated leukemia cell line expressed both ProteinE - cadherin transcript and protein. |
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| 0.9998 | Methylation | Our results show that DNA_methylationmethylation of ProteinE - cadherin occurs commonly in acute leukemia and suggests a hypothesis for E - cadherin down - regulation in leukemogenesis. |
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| 1.0000 | Methylation | GlycosylationHypoglycosylated forms of Proteinalpha1 - antitrypsin have been detected by Western blot in serum from CDG Ia patients. |
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| 1.0000 | Methylation | In contrast we were not able to detect Glycosylationhypoglycosylation in Proteinalpha1 - antitrypsin synthesized by fibroblasts, keratinocytes, enterocytes, and leukocytes. |
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| 0.9995 | Methylation | Similarly no Glycosylationhypoglycosylation was detectable in a membrane - associated N - linked glycoprotein, the facilitative glucose transporter ProteinGLUT - 1 and also in serum immunoglobulin G isolated from sera of CDG Ia patients. |
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| 0.9999 | Methylation | ProteinChM1L protein was expressed on the cell surface as GlycosylationN - glycosylated and non - N - glycosylated protein with molecular mass of 45 and 40 kDa, respectively. |
| 0.9987 | Methylation | ProteinChM1L protein was expressed on the cell surface as N - glycosylated and Glycosylationnon - N - glycosylated protein with molecular mass of 45 and 40 kDa, respectively. |
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| 0.8783 | Methylation | In oxygenated and iron replete cells, HIF - alpha subunits are rapidly destroyed by a mechanism that involves Ubiquitinationubiquitylation by the von ProteinHippel - Lindau tumor suppressor ( pVHL ) E3 ligase complex. |
| 0.6192 | Methylation | In oxygenated and iron replete cells, HIF - alpha subunits are rapidly destroyed by a mechanism that involves Ubiquitinationubiquitylation by the Proteinvon Hippel - Lindau tumor suppressor ( pVHL ) E3 ligase complex. |
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| 0.9980 | Methylation | Here we show that the interaction between human pVHL and a specific domain of the HIF - 1alpha subunit is regulated through Hydroxylationhydroxylation of a proline residue ( HIF - 1alpha EntityP564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ). |
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| 0.9979 | Methylation | We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for Entitypromoter DNA_methylationmethylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and hMSH6 genes. |
| 0.9610 | Methylation | We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for Entitypromoter DNA_methylationpromoter methylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and hMSH6 genes. |
| 0.8969 | Methylation | We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for DNA_methylationpromoter methylation DNA_methylationmethylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and hMSH6 genes. |
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| 0.9977 | Methylation | DNA_methylationHypermethylation of the hMLH1 Entitypromoter was observed in 6 ( 46 % ) of the 13 sporadic MSI - H tumors but not in any of the 3 hereditary MSI - H tumors or 13 MSI - L tumors. |
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| 0.9997 | Methylation | Synergism of Xist RNA, DNA methylation, and Proteinhistone Acetylationhypoacetylation in maintaining X chromosome inactivation. |
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| 0.9998 | Methylation | Xist RNA expression, methylation of CpG islands, and Acetylationhypoacetylation of Proteinhistone H4 are distinguishing features of inactive X chromatin. |
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| 0.9997 | Methylation | Demethylation of DNA, using 5 - azadC or by introducing a mutation in Dnmt1, and inhibition of Proteinhistone Acetylationhypoacetylation using trichostatin A further increases reactivation in Xist mutant fibroblasts, indicating a synergistic interaction of X chromosome silencing mechanisms. |
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| 0.9972 | Methylation | Expression of Pichia anomala ProteinINV1 gene in Saccharomyces cerevisiae results in two different active forms of Glycosylationhypoglycosylated invertase. |
| 0.9017 | Methylation | Expression of Pichia anomala ProteinINV1 gene in Saccharomyces cerevisiae results in two different active forms of Glycosylationhypoglycosylated invertase . |
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| 0.9994 | Methylation | Two forms of multimeric active and Glycosylationglycosylated Proteininvertase displaying different subcellular locations and molecular masses could be detected in the transformants. |
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| 0.9988 | Methylation | The Glycosylationhypoglycosylated Proteininvertase accumulated within the cells of the transformants to an unusual level ( up to 130 units / 10 ( 10 ) cells ). |
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| 1.0000 | Methylation | Such accumulation of active enzyme inside the cells, as well as its Glycosylationunderglycosylation , could be due to intrinsic properties of the P. anomala Proteininvertase that are determined by the particular primary structure of its protein moiety. |
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| 0.9999 | Methylation | The histone acetyltransferase, hGCN5, interacts with and Acetylationacetylates the HIV transactivator, ProteinTat . |
| 0.9996 | Methylation | The histone acetyltransferase, ProteinhGCN5 , interacts with and Acetylationacetylates the HIV transactivator, Tat. |
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| 0.9998 | Methylation | Here we report that hGCN5, a well known histone acetyltransferase, specifically interacts with and Acetylationacetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, ProteinTat . |
| 0.9976 | Methylation | Here we report that ProteinhGCN5 , a well known histone acetyltransferase, specifically interacts with and Acetylationacetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, Tat. |
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| 1.0000 | Methylation | Tat lysines 50 and Entity51 , target of Acetylationacetylation by p300 / CBP, were also found to be acetylated by hGCN5. |
| 0.9998 | Methylation | Tat lysines 50 and 51, target of acetylation by p300 / CBP, were also found to be Acetylationacetylated by ProteinhGCN5 . |
| 0.9980 | Methylation | Tat lysines 50 and Entity51 , target of acetylation by p300 / CBP, were also found to be Acetylationacetylated by hGCN5. |
| 0.9974 | Methylation | Tat Entitylysines 50 and 51, target of Acetylationacetylation by p300 / CBP, were also found to be acetylated by hGCN5. |
| 0.9837 | Methylation | Tat Entitylysines 50 and 51, target of acetylation by p300 / CBP, were also found to be Acetylationacetylated by hGCN5. |
| 0.9991 | Methylation | Tat lysines Entity50 and 51, target of Acetylationacetylation by p300 / CBP, were also found to be acetylated by hGCN5. |
| 0.9942 | Methylation | Tat lysines Entity50 and 51, target of acetylation by p300 / CBP, were also found to be Acetylationacetylated by hGCN5. |
| 0.9893 | Methylation | Tat Entitylysines 50 and 51, target of Acetylationacetylation by p300 / CBP, were also found to be acetylated by hGCN5. |
| 0.9396 | Methylation | Tat Entitylysines 50 and 51, target of acetylation by p300 / CBP, were also found to be Acetylationacetylated by hGCN5. |
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| 0.9998 | Methylation | The Acetylationacetylation of these two Entitylysines by p300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat. |
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| 1.0000 | Methylation | These data highlight the importance of the Acetylationacetylation of Entitylysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site. |
| 0.9989 | Methylation | These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, ProteinGCN5 and p300 / CBP, converge to Acetylationacetylate Tat on the same site. |
| 0.9986 | Methylation | These data highlight the importance of the acetylation of lysines 50 and Entity51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to Acetylationacetylate Tat on the same site. |
| 0.9957 | Methylation | These data highlight the importance of the Acetylationacetylation of lysines 50 and Entity51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site. |
| 0.9925 | Methylation | These data highlight the importance of the acetylation of Entitylysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to Acetylationacetylate Tat on the same site. |
| 0.9998 | Methylation | These data highlight the importance of the Acetylationacetylation of Entitylysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site. |
| 0.9657 | Methylation | These data highlight the importance of the acetylation of Entitylysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to Acetylationacetylate Tat on the same site. |
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| 0.9997 | Methylation | Furthermore, a - chains were Hydroxylationoverhydroxylated and the ratio of Proteinalpha1 ( I ) : alpha2 ( I ) was 3. 2 : 1, consistent with the presence of alpha1 ( I ) homotrimers. |
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| 0.9991 | Methylation | Linking global Proteinhistone Acetylationacetylation to the transcription enhancement of X - chromosomal genes in Drosophila males. |
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| 0.9997 | Methylation | It has become well established for several genes that targeting of Proteinhistone Acetylationacetylation to promoters is required for the activation of transcription. |
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| 0.9997 | Methylation | In Drosophila, a specific modification of H4, Acetylationacetylation at Entitylysine 16 , is enriched at hundreds of sites on the male X chromosome due to the activity of the male - specific lethal ( MSL ) dosage compensation complex. |
| 0.9985 | Methylation | In Drosophila, a specific modification of H4, Acetylationacetylation at Entitylysine 16, is enriched at hundreds of sites on the male X chromosome due to the activity of the male - specific lethal ( MSL ) dosage compensation complex. |
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| 0.9997 | Methylation | Utilizing chromatin immunoprecipitation, we have determined that ProteinH4Ac16 is present along the entire length of X - linked genes targeted by the MSL complex with relatively modest levels of Acetylationacetylation at the promoter regions and high levels in the middle and / or 3'end of the transcription units. |
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| 0.9996 | Methylation | MethylationMethylation of Proteinhistones at specific residues plays an important role in transcriptional regulation. |
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| 0.9308 | Methylation | Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated Entitylysine 9 Methylationmethylation and acetylation. |
| 0.9222 | Methylation | Chromatin immunoprecipitation of dimethylated lysine 9 on Proteinhistone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and Acetylationacetylation . |
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| Methylation | The amino - terminal ectodomain of the human TSH receptor has been expressed at the surface of CHO cells as a Entityglycosylphosphatidylinositol - anchored Entityglycosylphosphatidylinositol - anchored molecule containing a 10 - residue histidine tag close to its C terminus. | |
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| 1.0000 | Methylation | This allowed the identification of four out of the six potential EntityN - glycosylation sites as being effectively Glycosylationglycosylated . |
| 0.9992 | Methylation | This allowed the identification of four out of the six potential EntityN - glycosylation sites as being effectively Glycosylationglycosylated . |
| 0.4461 | Methylation | This allowed the identification of four out of the six potential EntityN - glycosylation sites EntityN - glycosylation sites as being effectively glycosylated. |
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| 0.9980 | Methylation | HIF - 1alpha binding to VHL is regulated by stimulus - sensitive Entityproline Hydroxylationhydroxylation . |
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| 0.9997 | Methylation | Through a combination of in vivo coimmunoprecipitation assays using VHL and a panel of point mutants of HIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is Hydroxylationhydroxylation of EntityPro - 564 of HIF - 1alpha. |
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| 0.9999 | Methylation | GlycosylationN - glycosylation of ProteinCRF receptor type 1 is important for its ligand - specific interaction. |
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| 0.9529 | Methylation | In vitro expression studies showed an influence of GlycosylationN - linked glycosylation Glycosylationglycosylation on expression efficiency, instability, and / or secretion of the mutated proteins. |
| 0.9435 | Methylation | In vitro expression studies showed an influence of GlycosylationN - linked glycosylation Glycosylationglycosylation on expression efficiency, instability, and / or secretion of the mutated proteins. |
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| 1.0000 | Methylation | These results show that GlycosylationN - linked glycosylation can limit the antibody response to the HCV ProteinE1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 1.0000 | Methylation | These results show that N - linked Glycosylationglycosylation can limit the antibody response to the HCV ProteinE1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 0.9965 | Methylation | These results show that GlycosylationN - linked glycosylation can limit the antibody response to the HCV ProteinE1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 0.8548 | Methylation | These results show that GlycosylationN - linked glycosylation Glycosylationglycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 0.8246 | Methylation | These results show that GlycosylationN - linked glycosylation Glycosylationglycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 0.7682 | Methylation | These results show that GlycosylationN - linked Glycosylationglycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 0.7531 | Methylation | These results show that GlycosylationN - linked GlycosylationN - linked glycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 0.6236 | Methylation | These results show that GlycosylationN - linked Glycosylationglycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
| 0.5492 | Methylation | These results show that GlycosylationN - linked glycosylation GlycosylationN - linked glycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity. |
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| Methylation | BAH null mice lack measurable BAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no Hydroxylationhydroxylation of the Entityepidermal growth factor ( EGF ) domain of clotting Factor X. | |
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| 0.9999 | Methylation | In this work, Hydroxylationbeta - hydroxylation of EntityAsp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human Jagged - 1. |
| 0.9997 | Methylation | In this work, Hydroxylationbeta - hydroxylation of EntityAsp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human Jagged - 1. |
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| 0.9982 | Methylation | Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in Proteinhistone Methylationmethylation , we tested the ability of ESET to methylate core histones. |
| 0.9999 | Methylation | Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone methylation, we tested the ability of ESET to Methylationmethylate core Proteinhistones . |
| 0.7511 | Methylation | Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone methylation, we tested the ability of ProteinESET to Methylationmethylate core histones. |
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| 0.9886 | Methylation | Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ProteinESET - mediated histone Methylationmethylation . |
| 0.5660 | Methylation | Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ProteinESET - mediated histone ProteinESET - mediated histone methylation. |
| 0.5367 | Methylation | Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ProteinESET - mediated ProteinESET - mediated histone methylation. |
| Methylation | Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ProteinESET - mediated ProteinESET - mediated histone methylation. | |
| Methylation | Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ESET - mediated Proteinhistone Methylationmethylation . | |
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| 0.9999 | Methylation | It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in Hydroxylationhydroxylation of at least one Entityprolyl residue ( HIF - 1alpha, Pro 564 ). |
| 0.9998 | Methylation | It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in Hydroxylationhydroxylation of at least one Entityprolyl residue ( HIF - 1alpha, Pro 564 ). |
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| 0.9993 | Methylation | EntityPromoter DNA_methylationmethylation status of the DNA repair genes hMLH1 and MGMT in gastric carcinoma and metaplastic mucosa. |
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| 0.9956 | Methylation | DNA repair genes human Mut L homologue 1 ( hMLH1 ) and ProteinO ( 6 ) - methylguanine - DNA methyltransferase ( MGMT ) have been shown to be DNA_methylationhypermethylated in certain carcinomas. |
| 0.9864 | Methylation | DNA repair genes human ProteinMut L homologue 1 ( hMLH1 ) and O ( 6 ) - methylguanine - DNA methyltransferase ( MGMT ) have been shown to be DNA_methylationhypermethylated in certain carcinomas. |
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| 1.0000 | Methylation | We studied DNA_methylationDNA methylation of EntityCpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples. |
| 1.0000 | Methylation | We studied DNA DNA_methylationmethylation of EntityCpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples. |
| 0.9745 | Methylation | We studied DNA_methylationDNA methylation of EntityCpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples. |
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| 0.9999 | Methylation | We analyzed the DNA_methylationmethylation status of ProteinhMLH1 and MGMT using methylation - specific polymerase chain reaction and DNA sequencing analysis. |
| 0.9998 | Methylation | We analyzed the DNA_methylationmethylation status of hMLH1 and ProteinMGMT using methylation - specific polymerase chain reaction and DNA sequencing analysis. |
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| 0.9906 | Methylation | EntityCpG island DNA_methylationhypermethylation of hMLH1 and MGMT was detected in 11 ( 22 % ) and 8 ( 16 % ) of the 50 gastric tumors, respectively. |
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| 0.9989 | Methylation | DNA_methylationHypermethylation of the Entitypromoter was more common in intestinal - type gastric carcinomas than in poorly diffuse - type gastric carcinomas ( p = 0. 016 and 0. 021, respectively ; Fisher's exact test ). |
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| 0.9955 | Methylation | However, hMLH1 Entitypromoter DNA_methylationhypermethylation did not coincide with MGMT promoter hypermethylation except in 1 patient. |
| 0.9932 | Methylation | However, hMLH1 promoter hypermethylation did not coincide with MGMT Entitypromoter DNA_methylationhypermethylation except in 1 patient. |
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| 0.9976 | Methylation | DNA_methylationHypermethylation of the hMLH1 Entitypromoter but not the MGMT promoter occurred in intestinal metaplastic mucosae. |
| 0.9921 | Methylation | DNA_methylationHypermethylation of the hMLH1 promoter but not the MGMT Entitypromoter occurred in intestinal metaplastic mucosae. |
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| 0.9972 | Methylation | Tumor - specific Entitypromoter DNA_methylationhypermethylation of hMLH1 may be an early event in carcinogenesis in the stomach. |
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| 1.0000 | Methylation | Together, histone acetyltransferases and histone deacetylases ( HDACs ) determine the Acetylationacetylation status of Proteinhistones . |
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| 1.0000 | Methylation | We found that the Proteinalpha ( 1B ) - AR undergoes GlycosylationN - linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.9999 | Methylation | We found that the Proteinalpha ( 1B ) - AR undergoes GlycosylationN - linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.9997 | Methylation | We found that the Proteinalpha ( 1B ) - AR undergoes N - linked Glycosylationglycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.8658 | Methylation | We found that the alpha ( 1B ) - AR undergoes GlycosylationN - linked glycosylation Glycosylationglycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.8465 | Methylation | We found that the alpha ( 1B ) - AR undergoes GlycosylationN - linked glycosylation Glycosylationglycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.8410 | Methylation | We found that the alpha ( 1B ) - AR undergoes GlycosylationN - linked Glycosylationglycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.8319 | Methylation | We found that the alpha ( 1B ) - AR undergoes GlycosylationN - linked GlycosylationN - linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.5566 | Methylation | We found that the alpha ( 1B ) - AR undergoes GlycosylationN - linked glycosylation GlycosylationN - linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
| 0.5341 | Methylation | We found that the alpha ( 1B ) - AR undergoes GlycosylationN - linked Glycosylationglycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. |
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| 1.0000 | Methylation | Pulse - chase labeling experiments in BHK - 21 cells demonstrate that the Proteinalpha ( 1B ) - AR is synthesized as a 70 kDa core Glycosylationglycosylated precursor that is converted to the 90 kDa mature form of the receptor with a half - time of approximately 2 h. |
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| 0.9977 | Methylation | N - Linked Glycosylationglycosylation of the alpha ( 1B ) - AR occurs at Entityfour asparagines on the N - terminus of the receptor. |
| 0.9988 | Methylation | N - Linked Glycosylationglycosylation of the alpha ( 1B ) - AR occurs at four Entityasparagines on the N - terminus of the receptor. |
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| 1.0000 | Methylation | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked glycosylation , contribute to the structural heterogeneity of the Proteinalpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.9993 | Methylation | Our findings demonstrate that GlycosylationN - linked glycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the Proteinalpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.9977 | Methylation | Our findings demonstrate that N - linked glycosylation and Phosphorylationphosphorylation , but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the Proteinalpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 1.0000 | Methylation | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or O - linked Glycosylationglycosylation , contribute to the structural heterogeneity of the Proteinalpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.9999 | Methylation | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked glycosylation, contribute to the structural heterogeneity of the Proteinalpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.9993 | Methylation | Our findings demonstrate that N - linked Glycosylationglycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the Proteinalpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.9981 | Methylation | Our findings demonstrate that GlycosylationN - linked glycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the Proteinalpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.7844 | Methylation | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked glycosylation Glycosylationglycosylation , contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.6685 | Methylation | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked glycosylation Glycosylationglycosylation , contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.6467 | Methylation | Our findings demonstrate that GlycosylationN - linked glycosylation Glycosylationglycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.5924 | Methylation | Our findings demonstrate that GlycosylationN - linked glycosylation Glycosylationglycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.5883 | Methylation | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked Glycosylationglycosylation , contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.5019 | Methylation | Our findings demonstrate that GlycosylationN - linked GlycosylationN - linked glycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.4980 | Methylation | Our findings demonstrate that GlycosylationN - linked Glycosylationglycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.4769 | Methylation | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked GlycosylationO - linked glycosylation , contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.4698 | Methylation | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked glycosylation GlycosylationO - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.4490 | Methylation | Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked Glycosylationglycosylation , contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
| 0.4099 | Methylation | Our findings demonstrate that GlycosylationN - linked Glycosylationglycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE. |
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| 0.9997 | Methylation | Our findings indicate that the Semliki Forest virus system can provide large amounts of functional and fully Glycosylationglycosylated Proteinalpha ( 1B ) - AR protein suitable for biochemical and structural studies. |
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| 0.9999 | Methylation | Binding mode analysis of 3 - ( 4 - benzoyl - 1 - methyl - 1H - 2 - pyrrolyl ) - N - hydroxy - 2 - propenamide : a new synthetic histone deacetylase inhibitor inducing Proteinhistone Acetylationhyperacetylation , growth inhibition, and terminal cell differentiation. |
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| 0.9997 | Methylation | Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced histone hyperacetylation leading to a highly increased Acetylationacetylation level of ProteinH4 as compared to control histones. |
| 0.9979 | Methylation | Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced Proteinhistone Acetylationhyperacetylation leading to a highly increased acetylation level of H4 as compared to control histones. |
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| 0.9999 | Methylation | The edge was methylated in 11 of 22 primary gastric cancers, whereas the Entitycenter was not DNA_methylationmethylated in any cancer. |
| 0.9993 | Methylation | The Entityedge was DNA_methylationmethylated in 11 of 22 primary gastric cancers, whereas the center was not methylated in any cancer. |
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| 0.9993 | Methylation | ProteinINSIG1 expression was markedly reduced in 19 cancers, including the 11 cancers with the DNA_methylationmethylation . |
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| 0.9999 | Methylation | By 5 - aza - 2'- deoxycytidine treatment of 5 cell lines with the DNA_methylationmethylation of the Entityedge , partial restoration of INSIG1 expression was detected only in 2 of them. |
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| 1.0000 | Methylation | These data indicated that, although the reduced INSIG1 expression in cancers was associated with the DNA_methylationmethylation at the Entityedge of the CGI in the promoter region, the methylation was likely to be a secondary change. |
| 0.9960 | Methylation | These data indicated that, although the reduced INSIG1 expression in cancers was associated with the DNA_methylationmethylation at the edge of the EntityCGI in the promoter region, the methylation was likely to be a secondary change. |
| 0.7434 | Methylation | These data indicated that, although the reduced INSIG1 expression in cancers was associated with the methylation at the Entityedge of the CGI in the promoter region, the DNA_methylationmethylation was likely to be a secondary change. |
| 0.6073 | Methylation | These data indicated that, although the reduced INSIG1 expression in cancers was associated with the methylation at the edge of the EntityCGI in the promoter region, the DNA_methylationmethylation was likely to be a secondary change. |
| Score | Relation | Text (Head - Tail) |
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| 1.0000 | Methylation | As for p41 - Arc, a DNA fragment was derived from a EntityCGI overlapping exon 8 , and its DNA_methylationmethylation did not correlate with its expression. |
| 1.0000 | Methylation | As for p41 - Arc, a DNA fragment was derived from a CGI overlapping Entityexon 8 , and its DNA_methylationmethylation did not correlate with its expression. |
| 1.0000 | Methylation | As for p41 - Arc, a DNA fragment was derived from a CGI Entityoverlapping exon 8 , and its DNA_methylationmethylation did not correlate with its expression. |
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| 0.9996 | Methylation | However, DNA_methylationmethylation of a EntityCGI in the promoter region with a marked reduction of its expression was observed in 1 of the 22 primary cancers. |
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| 0.9999 | Methylation | The kyphoscoliotic type of Ehlers - Danlos syndrome ( type VI ) : differential effects on the Hydroxylationhydroxylation of Entitylysine in collagens I and II revealed by analysis of cross - linked telopeptides from urine. |
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| 0.9986 | Methylation | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of alpha 1 ( I ) and Entity933 of alpha 2 ( I ) of the collagen triple - helix had not been Hydroxylationhydroxylated . |
| 0.9975 | Methylation | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at Entityresidues 930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been Hydroxylationhydroxylated . |
| 0.9976 | Methylation | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues Entity930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been Hydroxylationhydroxylated . |
| 0.9931 | Methylation | A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical Entitylysines at residues 930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been Hydroxylationhydroxylated . |
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| 0.9991 | Methylation | The results show that in EDS VIA, bone type I collagen is more markedly Glycosylationunderhydroxylated than cartilage Proteintype II collagen , at least at those helical sites that form cross - links. |
| Methylation | The results show that in EDS VIA, bone type I collagen is more markedly Hydroxylationunderhydroxylated than cartilage Proteintype II collagen , at least at those helical sites that form cross - links. | |
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| 0.9965 | Methylation | Postsynthetic Methylationtrimethylation of histone H4 at Entitylysine 20 in mammalian tissues is associated with aging. |
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| 0.9995 | Methylation | MethylationMethylation of the EntityN - terminal region of histones was first described more than 35 years ago, but its biological significance has remained unclear. |
| 0.9994 | Methylation | MethylationMethylation of the EntityN - terminal region of histones was first described more than 35 years ago, but its biological significance has remained unclear. |
| 0.5032 | Methylation | Methylation of the EntityN - terminal EntityN - terminal region of histones was first described more than 35 years ago, but its biological significance has remained unclear. |
| 0.4565 | Methylation | Methylation of the EntityN - terminal region EntityN - terminal region of histones was first described more than 35 years ago, but its biological significance has remained unclear. |
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| 0.9998 | Methylation | Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and ProteinSuv39h1 , which selectively Methylationmethylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.9987 | Methylation | Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases ProteinSUV39H1 and Suv39h1, which selectively Methylationmethylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.9927 | Methylation | Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively Methylationmethylate Entitylysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
| 0.9733 | Methylation | Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively Methylationmethylate Entitylysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest. |
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| 0.9999 | Methylation | In the past, investigations concerning the biological significance of Proteinhistone Methylationmethylation were largely limited because of a lack of simple and sensitive analytical procedures for detecting this modification. |
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| 1.0000 | Methylation | The present work investigated the Methylationmethylation pattern of Proteinhistone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of methylated and acetylated forms, which obviates the need to work with radioactive materials. |
| 0.7415 | Methylation | The present work investigated the methylation pattern of Proteinhistone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of methylated and Acetylationacetylated forms, which obviates the need to work with radioactive materials. |
| 0.5063 | Methylation | The present work investigated the methylation pattern of Proteinhistone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of Methylationmethylated and acetylated forms, which obviates the need to work with radioactive materials. |
| Score | Relation | Text (Head - Tail) |
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| 0.9987 | Methylation | In rat kidney and liver the Methylationdimethylated Entitylysine 20 was found to be the main methylation product, whereas the monomethyl derivative was present in much smaller amounts. |
| 0.9987 | Methylation | In rat kidney and liver the dimethylated Entitylysine 20 was found to be the main methylation product, whereas the Methylationmonomethyl derivative was present in much smaller amounts. |
| 0.9999 | Methylation | In rat kidney and liver the dimethylated Entitylysine 20 was found to be the main Methylationmethylation product, whereas the monomethyl derivative was present in much smaller amounts. |
| 0.9964 | Methylation | In rat kidney and liver the dimethylated Entitylysine 20 was found to be the main Methylationmethylation product, whereas the monomethyl derivative was present in much smaller amounts. |
| 0.9956 | Methylation | In rat kidney and liver the Methylationdimethylated Entitylysine 20 was found to be the main methylation product, whereas the monomethyl derivative was present in much smaller amounts. |
| 0.9810 | Methylation | In rat kidney and liver the dimethylated Entitylysine 20 was found to be the main methylation product, whereas the Methylationmonomethyl derivative was present in much smaller amounts. |
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| 0.9998 | Methylation | In addition, for the first time a Methylationtrimethylated form of Entitylysine 20 of H4 was found in mammalian tissue. |
| 0.9992 | Methylation | In addition, for the first time a Methylationtrimethylated form of Entitylysine 20 of H4 was found in mammalian tissue. |
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| 0.9995 | Methylation | A significant increase in this trimethylated Proteinhistone H4 was detected in organs of animals older than 30 days, whereas the amounts of Methylationmono - and dimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ). |
| 0.9994 | Methylation | A significant increase in this Methylationtrimethylated Proteinhistone H4 was detected in organs of animals older than 30 days, whereas the amounts of mono - and dimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ). |
| 0.9991 | Methylation | A significant increase in this trimethylated Proteinhistone H4 was detected in organs of animals older than 30 days, whereas the amounts of mono - and Methylationdimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ). |
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| 0.9982 | Methylation | MethylationTrimethylated ProteinH4 was also detected in transformed cells ; although it was present in only trace amounts in logarithmically growing cells, we found an increase in trimethylated lysine 20 in cells in the stationary phase. |
| 0.9844 | Methylation | Trimethylated H4 was also detected in transformed cells ; although it was present in only trace amounts in logarithmically growing cells, we found an increase in Methylationtrimethylated Entitylysine 20 in cells in the stationary phase. |
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| 0.9997 | Methylation | GlycosylationGlycosylation of human Proteinproteinase - activated receptor - 2 ( hPAR2 ) : role in cell surface expression and signalling. |
| Score | Relation | Text (Head - Tail) |
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| 0.9999 | Methylation | We have analysed the role of GlycosylationN - linked glycosylation in regulating human Proteinproteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.9998 | Methylation | We have analysed the role of N - linked Glycosylationglycosylation in regulating human Proteinproteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.9393 | Methylation | We have analysed the role of GlycosylationN - linked glycosylation in regulating human Proteinproteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.8599 | Methylation | We have analysed the role of GlycosylationN - linked glycosylation Glycosylationglycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.8415 | Methylation | We have analysed the role of GlycosylationN - linked glycosylation Glycosylationglycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.8291 | Methylation | We have analysed the role of GlycosylationN - linked GlycosylationN - linked glycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.8230 | Methylation | We have analysed the role of GlycosylationN - linked Glycosylationglycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.6961 | Methylation | We have analysed the role of GlycosylationN - linked Glycosylationglycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
| 0.6738 | Methylation | We have analysed the role of GlycosylationN - linked glycosylation GlycosylationN - linked glycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function. |
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| 0.9993 | Methylation | Western blot analysis of wt - hPAR ( 2 ) showed mature Proteinwt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N - glycosidase F Catalysisdeglycosylation . |
| 0.9958 | Methylation | Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N Protein- glycosidase F Catalysisdeglycosylation . |
| 0.9956 | Methylation | Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following ProteinN - glycosidase F Catalysisdeglycosylation . |
| Methylation | Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following ProteinN - glycosidase F Deglycosylationdeglycosylation . | |
| Methylation | Western blot analysis of wt - hPAR ( 2 ) showed mature Proteinwt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N - glycosidase F Deglycosylationdeglycosylation . | |
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| 0.9999 | Methylation | Western blot analysis indicated that both EntityN - linked sites are Glycosylationglycosylated . |
| 0.9979 | Methylation | Western blot analysis indicated that both EntityN - linked sites are Glycosylationglycosylated . |
| 0.4813 | Methylation | Western blot analysis indicated that both EntityN - linked sites EntityN - linked sites are glycosylated. |
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| 0.9991 | Methylation | We conclude that ProteinhPAR ( 2 ) GlycosylationN - linked glycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.9956 | Methylation | We conclude that ProteinhPAR ( 2 ) GlycosylationN - linked glycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.9867 | Methylation | We conclude that ProteinhPAR ( 2 ) N - linked Glycosylationglycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.9268 | Methylation | We conclude that hPAR ( 2 ) GlycosylationN - linked glycosylation Glycosylationglycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.9242 | Methylation | We conclude that hPAR ( 2 ) GlycosylationN - linked Glycosylationglycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.8991 | Methylation | We conclude that hPAR ( 2 ) GlycosylationN - linked glycosylation Glycosylationglycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.8932 | Methylation | We conclude that hPAR ( 2 ) GlycosylationN - linked GlycosylationN - linked glycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.6459 | Methylation | We conclude that hPAR ( 2 ) GlycosylationN - linked Glycosylationglycosylation and sialylation regulates receptor expression and / or signalling. |
| 0.6401 | Methylation | We conclude that hPAR ( 2 ) GlycosylationN - linked glycosylation GlycosylationN - linked glycosylation and sialylation regulates receptor expression and / or signalling. |
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| 0.9988 | Methylation | Histone H3 lysine 4 methylation is Catalysismediated by ProteinSet1 and promotes maintenance of active chromatin states in fission yeast. |
| 0.9803 | Methylation | Histone H3 Entitylysine 4 Methylationmethylation is mediated by Set1 and promotes maintenance of active chromatin states in fission yeast. |
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| 0.9951 | Methylation | MethylationMethylation of histone H3 at Entitylysine 4 ( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
| 0.9914 | Methylation | MethylationMethylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or Entitylysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans. |
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| 0.9993 | Methylation | However, in budding yeast, H3 EntityLys - 4 Methylationmethylation is also necessary for silent chromatin assembly at telomeres and ribosomal DNA. |
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| 0.9979 | Methylation | Here we demonstrate that deletion of set1, which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes H3 EntityLys - 4 Methylationmethylation in fission yeast. |
| 0.9305 | Methylation | Here we demonstrate that deletion of set1, which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes EntityH3 Lys - 4 Methylationmethylation in fission yeast. |
| Score | Relation | Text (Head - Tail) |
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| 0.9759 | Methylation | Unlike in budding yeast, Set1 - mediated H3 EntityLys - 4 Methylationmethylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast. |
| 0.6041 | Methylation | Unlike in budding yeast, CatalysisSet1 - mediated ProteinSet1 - mediated H3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast. |
| 0.5512 | Methylation | Unlike in budding yeast, ProteinSet1 - mediated H3 CatalysisSet1 - mediated H3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast. |
| Methylation | Unlike in budding yeast, ProteinSet1 - mediated ProteinSet1 - mediated H3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast. | |
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| 0.9973 | Methylation | Our analysis suggests that H3 EntityLys - 4 Methylationmethylation is a stable histone modification present throughout the cell cycle, including mitosis. |
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| 0.9946 | Methylation | The loss of H3 EntityLys - 4 Methylationmethylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail. |
| 0.9913 | Methylation | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 EntityLys - 4 Methylationmethylation and acetylation of the H3 tail. |
| 0.9854 | Methylation | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and Acetylationacetylation of the H3 Entitytail . |
| 0.9851 | Methylation | The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in Proteinhistone H3 Acetylationacetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail. |
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| 0.9987 | Methylation | We suggest that methylation of H3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 EntityLys - 9 Methylationmethylation . |
| 0.9942 | Methylation | We suggest that Methylationmethylation of H3 EntityLys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 Lys - 9 methylation. |
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| 0.9993 | Methylation | Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is Hydroxylationhydroxylated by Proteinfactor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction. |
| 0.9951 | Methylation | EntityAsparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is Hydroxylationhydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction. |
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| 0.9994 | Methylation | NMR and other analyses of a hydroxylated HIF fragment produced in vitro demonstrate that Hydroxylationhydroxylation occurs at the beta - carbon of EntityAsn - 803 and imply production of the threo - isomer, in contrast with other known aspartic acid / asparagine hydroxylases that produce the erythro - isomer. |
| 0.5956 | Methylation | NMR and other analyses of a Hydroxylationhydroxylated HIF fragment produced in vitro demonstrate that hydroxylation occurs at the beta - carbon of EntityAsn - 803 and imply production of the threo - isomer, in contrast with other known aspartic acid / asparagine hydroxylases that produce the erythro - isomer. |
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| 0.9998 | Methylation | Control of CBP co - activating activity by Entityarginine Methylationmethylation . |
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| 1.0000 | Methylation | Recently, the KIX domain of CBP has been shown to be Catalysismethylated by ProteinCARM1 in vitro. |
| 0.9985 | Methylation | Recently, the EntityKIX domain of CBP has been shown to be Catalysismethylated by CARM1 in vitro. |
| 0.9883 | Methylation | Recently, the EntityKIX domain of CBP has been shown to be Catalysismethylated by CARM1 in vitro. |
| Methylation | Recently, the EntityKIX domain of CBP has been shown to be Methylationmethylated by CARM1 in vitro. | |
| Methylation | Recently, the KIX domain of CBP has been shown to be Methylationmethylated by ProteinCARM1 in vitro. | |
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| 1.0000 | Methylation | Here, we report that another domain of CBP is specifically Catalysismethylated by ProteinCARM1 on conserved arginine residues in vitro and in vivo. |
| 1.0000 | Methylation | Here, we report that another domain of ProteinCBP is specifically Catalysismethylated by CARM1 on conserved arginine residues in vitro and in vivo. |
| Methylation | Here, we report that another domain of CBP is specifically Methylationmethylated by ProteinCARM1 on conserved arginine residues in vitro and in vivo. | |
| Methylation | Here, we report that another domain of ProteinCBP is specifically Methylationmethylated by CARM1 on conserved arginine residues in vitro and in vivo. | |
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| 0.9999 | Methylation | We also provide functional evidence that arginine residues Methylationmethylated by ProteinCARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation. |
| 0.9997 | Methylation | We also provide functional evidence that Entityarginine residues Methylationmethylated by CARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation. |
| 0.9928 | Methylation | We also provide functional evidence that Entityarginine residues Methylationmethylated by CARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation. |
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| 0.9990 | Methylation | Gene - specific targeting of EntityH3K9 Methylationmethylation is sufficient for initiating repression in vivo. |
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| 0.9982 | Methylation | Histone H3 Entitylysine 9 ( H3K9 ) Methylationmethylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms. |
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| 0.9989 | Methylation | Discovery of the enzymes that catalyze EntityH3K9 Methylationmethylation has identified a second gene - specific function for this modification in transcriptional repression. |
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| 0.9991 | Methylation | Whether EntityH3K9 Methylationmethylation is causative in the initiation and establishment of gene repression or is a byproduct of the process leading to the repressed state remains unknown. |
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| 0.9996 | Methylation | To investigate the role of HMTs and specifically EntityH3K9 Methylationmethylation in gene repression, we have employed engineered zinc - finger transcription factors ( ZFPs ) to target HMT activity to a specific endogenous gene. |
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| 0.9991 | Methylation | Thus, EntityH3K9 Methylationmethylation is a primary signal that is sufficient for initiating a gene repression pathway in vivo. |
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| 1.0000 | Methylation | These bind to, and activate, co - activator molecules that then Acetylationacetylate core Proteinhistones resulting in elevated gene transcription. |
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| 0.9992 | Methylation | Corticosteroids reverse Proteinhistone Acetylationacetylation at the site of inflammatory gene transcription, either by direct binding of the activated glucocorticoid receptor to NF - kappa B - associated co - activators or by recruitment of histone deacetylases to the activated transcription complex. |
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| 1.0000 | Methylation | Probing the conformational and dynamical effects of GlycosylationO - glycosylation within the Entityimmunodominant region of a MUC1 peptide tumor antigen. |
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| 0.9952 | Methylation | However, in neoplastic breast tissue, the Glycosylationextracellular Entitydomain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates. |
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| 0.9996 | Methylation | The results of these studies show that a type I beta - turn conformation is adopted by residues PDTR within the PDTRP region of the Glycosylationunglycosylated ProteinMUC1 sequence. |
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| 0.9999 | Methylation | The existence of a similar beta - turn within the PDTRP core peptide Entityepitope of the Glycosylationunder - glycosylated cancer - associated MUC1 mucin protein might explain the immunodominance of this region in vivo, as the presence of defined secondary structure within peptide epitope regions has been correlated with increased immunogenicity in other systems. |
| Methylation | The existence of a similar beta - turn within the EntityPDTRP core peptide epitope of the Glycosylationunder - glycosylated cancer - associated MUC1 mucin protein might explain the immunodominance of this region in vivo, as the presence of defined secondary structure within peptide epitope regions has been correlated with increased immunogenicity in other systems. | |
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| 0.9999 | Methylation | The significance of these results are discussed in relation to the possible roles that peptide epitope secondary structure and Glycosylationglycosylation state may play in ProteinMUC1 tumor immunogenicity. |
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| 0.9968 | Methylation | EntityLysine - 79 of histone H3 is Methylationhypomethylated at silenced loci in yeast and mammalian cells : a potential mechanism for position - effect variegation. |
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| 0.9994 | Methylation | MethylationMethylation of Entitylysine - 79 ( K79 ) within the globular domain of histone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast. |
| 0.9926 | Methylation | MethylationMethylation of lysine - 79 ( K79 ) within the globular domain of histone H3 by ProteinDot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast. |
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| 0.9991 | Methylation | Here, we show that the level of EntityH3 - K79 Methylationmethylation is low at all Sir - dependent silenced loci but not at other transcriptionally repressed regions. |
| Methylation | Here, we show that the level of ProteinH3 - K79 Methylationmethylation is low at all Sir - dependent silenced loci but not at other transcriptionally repressed regions. | |
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| 1.0000 | Methylation | MethylationHypomethylation of ProteinH3 - K79 at the telomeric and silent mating - type loci, but not the ribosomal DNA, requires the Sir proteins. |
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| 0.9994 | Methylation | Overexpression of Sir3 concomitantly extends the domain of Sir protein association and EntityH3 - K79 Methylationhypomethylation at telomeres. |
| Methylation | Overexpression of Sir3 concomitantly extends the domain of Sir protein association and ProteinH3 - K79 Methylationhypomethylation at telomeres. | |
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| 0.9996 | Methylation | In mammalian cells, EntityH3 - K79 Methylationmethylation is found at loci that are active for V ( D ) J recombination, but not at recombinationally inactive loci that are heterochromatic. |
| Methylation | In mammalian cells, ProteinH3 - K79 Methylationmethylation is found at loci that are active for V ( D ) J recombination, but not at recombinationally inactive loci that are heterochromatic. | |
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| 0.9989 | Methylation | These results suggest that H3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of ProteinDot1 to Methylationmethylate histone H3. |
| 0.9968 | Methylation | These results suggest that ProteinH3 - K79 Methylationmethylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to methylate histone H3. |
| 0.9967 | Methylation | These results suggest that H3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to Methylationmethylate Proteinhistone H3 . |
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| 0.9969 | Methylation | Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated H3 - K79 and then block EntityH3 - K79 Methylationmethylation . |
| 0.9873 | Methylation | Further, they suggest that Sir proteins preferentially bind chromatin with Methylationhypomethylated EntityH3 - K79 and then block H3 - K79 methylation. |
| Methylation | Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated H3 - K79 and then block ProteinH3 - K79 Methylationmethylation . | |
| Methylation | Further, they suggest that Sir proteins preferentially bind chromatin with Methylationhypomethylated ProteinH3 - K79 and then block H3 - K79 methylation. | |
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| 0.9995 | Methylation | This positive feedback loop, and the reverse loop in which ProteinH3 - K79 Methylationmethylation weakens Sir protein association and leads to further methylation, suggests a model for position - effect variegation. |
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| 0.9987 | Methylation | Cyclosporin A prevents the hypoxic adaptation by activating hypoxia - inducible factor - 1alpha EntityPro - 564 Hydroxylationhydroxylation . |
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| 0.9999 | Methylation | We conclude that CsA destabilizes HIF - 1alpha by promoting Hydroxylationhydroxylation of EntityPro - 564 in the ODD domain. |
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| 0.9998 | Methylation | Preclinical evaluation of antineoplastic activity of inhibitors of DNA methylation ( 5 - aza - 2'- deoxycytidine ) and Proteinhistone Deacetylationdeacetylation ( trichostatin A, depsipeptide ) in combination against myeloid leukemic cells. |
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| 0.9999 | Methylation | During the development of leukemia, genes that suppress growth and induce differentiation can be silenced by aberrant DNA methylation and by changes in chromatin structure that involve Proteinhistone Deacetylationdeacetylation . |
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| 0.9998 | Methylation | It has been reported that a positive interaction between DNA methylation and Proteinhistone Deacetylationdeacetylation takes place to inhibit transcription. |
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| 1.0000 | Methylation | Surprisingly, dystroglycan was cleaved, and Proteinalpha dystroglycan was Glycosylationglycosylated with the VIA4 - 1 antigen, in DG ( S654A ) / CT muscles. |
| 1.0000 | Methylation | Surprisingly, dystroglycan was cleaved, and alpha Proteindystroglycan was Glycosylationglycosylated with the VIA4 - 1 antigen, in DG ( S654A ) / CT muscles. |
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| 0.9998 | Methylation | NgRH1 and ProteinNgRH2 were detected on the cell surface of recombinant cell lines as GlycosylationN - glycosylated GPI anchored proteins and, consistent with other GPI anchored proteins, were localized within the lipid rafts of cellular membranes. |
| 0.9995 | Methylation | ProteinNgRH1 and NgRH2 were detected on the cell surface of recombinant cell lines as GlycosylationN - glycosylated GPI anchored proteins and, consistent with other GPI anchored proteins, were localized within the lipid rafts of cellular membranes. |
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| 0.9999 | Methylation | Transcriptional elongation by RNA polymerase II and Proteinhistone Methylationmethylation . |
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| 0.9996 | Methylation | In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to Proteinhistone Methylationmethylation by COMPASS, Dot1p, and Set2 methyltransferases. |
| 0.9995 | Methylation | In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to histone Methylationmethylation by COMPASS, ProteinDot1p , and Set2 methyltransferases. |
| 0.9991 | Methylation | In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to histone Methylationmethylation by COMPASS, Dot1p, and ProteinSet2 methyltransferases. |
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| 0.9976 | Methylation | Occurrence of GlycosylationO - linked Xyl - GlcNAc and EntityXyl - Glc disaccharides in trocarin, a factor Xa homolog from snake venom. |
| 0.9955 | Methylation | Occurrence of GlycosylationO - linked EntityXyl - GlcNAc and Xyl - Glc disaccharides in trocarin, a factor Xa homolog from snake venom. |
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| 0.9999 | Methylation | In this study we show that, in contrast to mammalian ProteinXa , which is not Glycosylationglycosylated , trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.9902 | Methylation | In this study we show that, in contrast to mammalian ProteinXa , which is not glycosylated, trocarin contains an GlycosylationO - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain. |
| 0.9809 | Methylation | In this study we show that, in contrast to mammalian ProteinXa , which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an GlycosylationN - linked carbohydrate oligosaccharide in its heavy chain. |
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| 0.6108 | Methylation | The GlycosylationN - linked Entitycarbohydrate on Asn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator. |
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| 0.9991 | Methylation | Here we show that ProteinLRP1 is differentially Glycosylationglycosylated in a tissue - specific manner and that carbohydrate addition reduces proteolytic cleavage of the extracellular domain and, concomitantly, ICD release. |
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| 0.9996 | Methylation | Bone marrow or peripheral blood samples from 48 patients with leukemia were examined by multiplex polymerase chain reaction ( MPCR ) to detect p16 gene homozygous deletion, and restriction enzyme PCR to detect Proteinp16 gene DNA_methylationmethylation . p16 gene inactivation were detected in 10 of the 48 patients ( 20. 4 % ). |
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| 0.9992 | Methylation | They were five patients with p16 homozygous deletion, and five patients with Proteinp16 DNA_methylationmethylation , respectively. p16 gene inactivation correlates with adverse prognosis features. |
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| 1.0000 | Methylation | The MENT distribution profile was opposite to that of Acetylationacetylated core Proteinhistones but correlated with that of histone H3 dimethylated at lysine 9 ( H3me2K9 ). |
| 0.9996 | Methylation | The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 Methylationdimethylated at Entitylysine 9 ( H3me2K9 ). |
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| 0.9997 | Methylation | Mutational analysis of MENT and experiments with deacetylase inhibitors revealed the essential role of the reaction center loop domain and an inhibitory affect of Proteinhistone Acetylationhyperacetylation on the MENT - induced chromatin remodeling in vivo. |
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| 0.9995 | Methylation | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not Acetylationacetylated EntityN - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
| 0.9987 | Methylation | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with Methylationdimethylated but not acetylated EntityN - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
| 0.9994 | Methylation | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not Acetylationacetylated EntityN - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
| 0.9985 | Methylation | In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with Methylationdimethylated but not acetylated EntityN - terminal domain of histone H3 specifically restored chromatin self - association by MENT. |
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| 0.9991 | Methylation | We suggest that histone H3 modification at lysine 9 directly regulates chromatin condensation by recruiting MENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and Proteinhistone Acetylationhyperacetylation . |
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| 0.9999 | Methylation | ProteinHistone Acetylationhyperacetylation in mitosis prevents sister chromatid separation and produces chromosome segregation defects. |
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| 0.9997 | Methylation | Herein, we investigated the role of Proteinhistone Deacetylationdeacetylation on the mitotic process by inhibiting histone deacetylases shortly before mitosis in human primary fibroblasts. |
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| 0.9992 | Methylation | Cells entering mitosis with Acetylationhyperacetylated Proteinhistones displayed altered chromatin conformation associated with decreased reactivity to the anti - Ser 10 phospho H3 antibody, increased recruitment of protein phosphatase 1 - delta on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin. |
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| 0.9998 | Methylation | Inhibition of Proteinhistone Deacetylationdeacetylation before mitosis produced defective chromosome condensation and impaired mitotic progression in living cells, suggesting that improper chromosome condensation may induce mitotic checkpoint activation. |
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| 0.9989 | Methylation | Lagging chromosomes consisting of single or paired sisters were also induced by the presence of Acetylationhyperacetylated Proteinhistones , indicating that the less constrained centromeric organization associated with heterochromatin protein 1 depletion may promote the attachment of kinetochores to microtubules coming from both poles. |
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| 0.9982 | Methylation | HydroxylationHydroxylated kininogens and Proteinkinins . |
| 0.9981 | Methylation | HydroxylationHydroxylated Proteinkininogens and kinins. |
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| 0.9989 | Methylation | The present results and our previous results indicate that only Proteinkinin moity in H kininogen from human and monkey plasmas has been partially Hydroxylationhydroxylated post - translationally by proline - 4 - hydroxylase. |
| 0.4434 | Methylation | The present results and our previous results indicate that only kinin moity in H kininogen from human and monkey plasmas has been partially Hydroxylationhydroxylated post - translationally by Proteinproline - 4 - hydroxylase . |
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| 0.9995 | Methylation | The ProteinSCFs expressed in CHO cells are secreted into the medium in active state and, like the natural SCF, are Glycosylationglycosylated . |
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| 0.9984 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites in HN, which are Glycosylationutilized and presumably account for the escape from neutralization. |
| 0.9991 | Methylation | Some of the deduced amino acid substitutions result in additional N - linked Entityglycosylation sites in HN, which are Glycosylationutilized and presumably account for the escape from neutralization. |
| 0.9970 | Methylation | Some of the deduced amino acid substitutions result in additional N - linked Entityglycosylation sites in HN, which are Glycosylationutilized and presumably account for the escape from neutralization. |
| 0.9945 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites in HN, which are Glycosylationutilized and presumably account for the escape from neutralization. |
| 0.9625 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites in HN, which are Glycosylationutilized and presumably account for the escape from neutralization. |
| 0.8151 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.8138 | Methylation | Some of the deduced amino acid substitutions result in additional N - linked Entityglycosylation sites Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.8119 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.7828 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.7171 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites EntityN - linked glycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.7153 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.7102 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.6894 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.6849 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.6821 | Methylation | Some of the deduced amino acid substitutions result in additional N - linked Entityglycosylation Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.6746 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites EntityN - linked glycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.6448 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.5407 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.5377 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation EntityN - linked glycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.5345 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
| 0.4927 | Methylation | Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation EntityN - linked glycosylation sites in HN, which are utilized and presumably account for the escape from neutralization. |
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| 0.9999 | Methylation | The influence of GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of rubella virus ProteinE1 glycoprotein. |
| 0.9999 | Methylation | The influence of N - linked Glycosylationglycosylation on the antigenicity and immunogenicity of rubella virus ProteinE1 glycoprotein. |
| 0.8685 | Methylation | The influence of GlycosylationN - linked glycosylation Glycosylationglycosylation on the antigenicity and immunogenicity of rubella virus E1 glycoprotein. |
| 0.8347 | Methylation | The influence of GlycosylationN - linked glycosylation Glycosylationglycosylation on the antigenicity and immunogenicity of rubella virus E1 glycoprotein. |
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| 0.9999 | Methylation | The role of GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of ProteinE1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.9999 | Methylation | The role of N - linked Glycosylationglycosylation on the antigenicity and immunogenicity of ProteinE1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.9783 | Methylation | The role of GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of ProteinE1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.8596 | Methylation | The role of GlycosylationN - linked glycosylation Glycosylationglycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.7845 | Methylation | The role of GlycosylationN - linked glycosylation Glycosylationglycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.7073 | Methylation | The role of GlycosylationN - linked Glycosylationglycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.6493 | Methylation | The role of GlycosylationN - linked GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.6315 | Methylation | The role of GlycosylationN - linked Glycosylationglycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
| 0.6080 | Methylation | The role of GlycosylationN - linked glycosylation GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants. |
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| 0.9996 | Methylation | GlycosylationGlycosylation of the Proteininterleukin - 1 receptor type I is required for optimal binding of interleukin - 1. |
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| 0.9996 | Methylation | To determine the role of Glycosylationglycosylation of the ProteinIL - 1 receptor type I ( IL - 1RtI ) in the binding and function of IL - 1, we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for IL - 1. |
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| 0.9923 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the ProteinIL - 1RtI is due to N - linked carbohydrates, that the degree of Glycosylationglycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.9541 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the ProteinIL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.8956 | Methylation | This study demonstrates that Glycosylationglycosylation of the extracellular domain of the IL - 1RtI is due to N - linked Entitycarbohydrates , that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.9473 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the ProteinIL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked Glycosylationglycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.9015 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the ProteinIL - 1RtI is due to GlycosylationN - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.8832 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the ProteinIL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.8784 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked glycosylation Glycosylationglycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.8477 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked glycosylation Glycosylationglycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.7924 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked Glycosylationglycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.7901 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked GlycosylationN - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.7245 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked Glycosylationglycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
| 0.6665 | Methylation | This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked glycosylation GlycosylationN - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor. |
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| 0.9986 | Methylation | However, the function of these antigens appears to be dependent on the presence of multiple GlycosylationO - linked Entityalpha - N - acetylgalactosamine ( alpha - GalNAc ) determinants. |
| 0.8171 | Methylation | However, the function of these antigens appears to be dependent on the presence of multiple GlycosylationO - linked Entityalpha - N - acetylgalactosamine ( alpha - GalNAc ) determinants. |
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| 0.9982 | Methylation | The presence of terminal GlycosylationO - linked Entityalpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes alpha - GalNAc residues, and digestion with alpha - N - acetylgalactosaminidase. |
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| 1.0000 | Methylation | Aberrant DNA_methylationmethylation of ProteinDAP - kinase in therapy - related acute myeloid leukemia and myelodysplastic syndromes. |
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| 1.0000 | Methylation | We studied the DNA_methylationmethylation status of ProteinDAP - kinase of 194 bone marrow samples from 160 patients with acute myeloid leukemia ( AML ) and 34 with a myelodysplastic syndrome ( MDS ) at the time of initial diagnosis by polymerase chain reaction ( PCR ). |
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| 0.9999 | Methylation | DNA_methylationHypermethylation of ProteinDAP - kinase was present in 27. 5 % ( 44 of 160 ) of AML and in 47 % ( 16 of 34 ) of MDS specimens and significantly correlated to loss of DAP - kinase expression ( P =. 008 ). |
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| 0.9998 | Methylation | ProteinDAP - kinase DNA_methylationhypermethylation in AML was associated with myelodysplastic changes in the bone marrow at the time of the initial diagnosis ( P =. 002 ) and with the presence of cytogenetic abnormalities ( P =. 02 ). |
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| 0.9941 | Methylation | DNA from paraffin - embedded tissue of 6 APAs was evaluated for microsatellite instability ( MI ), MLH - 1 Entitypromoter DNA_methylationhypermethylation , and CTNNB - 1 mutations. |
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| 0.9944 | Methylation | Two tumors exhibited MLH - 1 Entitypromoter DNA_methylationhypermethylation and showed focal negative MHL - 1 immunostaining ; 1 of these showed marked architectural complexity and cellular pleomorphism. |
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| 0.9973 | Methylation | Some APAs exhibit MLH - 1 Entitypromoter DNA_methylationhypermethylation with focal lack of MLH - 1 immunostaining, a molecular abnormality involved in the transition from complex atypical hyperplasia to endometrioid adenocarcinoma. |
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| 0.9986 | Methylation | A common polymorphism in the oxygen - dependent degradation ( ODD ) domain of hypoxia inducible factor - 1alpha ( HIF - 1alpha ) does not impair EntityPro - 564 Hydroxylationhydroxylation . |
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| 1.0000 | Methylation | Under normoxic conditions, the alpha subunit of HIF is rapidly degraded in a manner dependent on Hydroxylationhydroxylation of two conserved Entityproline residues at positions 402 and 564 in HIF - 1alpha in the oxygen - dependent degradation ( ODD ) domain. |
| 0.9999 | Methylation | Under normoxic conditions, the alpha subunit of HIF is rapidly degraded in a manner dependent on Hydroxylationhydroxylation of two conserved Entityproline residues at positions 402 and 564 in HIF - 1alpha in the oxygen - dependent degradation ( ODD ) domain. |
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| 0.9975 | Methylation | CONCLUSION : The Pro582Ser change represents a common polymorphism of HIF - 1alpha that does not impair HIF - 1alpha Entityprolyl Hydroxylationhydroxylation . |
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| 0.9999 | Methylation | When Deglycosylationdeglycosylated , the protein displayed the molecular weight expected for the longest ProteinCLECSF6 form. |
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| 0.9999 | Methylation | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine DNA_methylationmethylation restricted to the Entity3'end and center part of the transcribed region. |
| 0.9997 | Methylation | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine DNA_methylationmethylation restricted to the 3'end and Entitycenter part of the transcribed region. |
| 0.9999 | Methylation | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine DNA_methylationmethylation restricted to the 3 ' Entityend and center part of the transcribed region. |
| 0.9999 | Methylation | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine DNA_methylationmethylation restricted to the Entity3 ' end and center part of the transcribed region. |
| 0.9997 | Methylation | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine DNA_methylationmethylation restricted to the 3'end and center part of the Entitytranscribed region . |
| 0.9994 | Methylation | Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine DNA_methylationmethylation restricted to the 3'end and Entitycenter part of the transcribed region. |
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| 0.9998 | Methylation | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine DNA_methylationmethylation of symmetrical ( CG and CNG ) sites was almost complete within the Entity5'end of the nptII - transcribed region and the 35S promoter. |
| 0.9986 | Methylation | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine DNA_methylationmethylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the Entity35S promoter . |
| 0.9997 | Methylation | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine DNA_methylationmethylation of symmetrical ( CG and CNG ) sites was almost complete within the Entity5 ' end of the nptII - transcribed region and the 35S promoter. |
| 0.9997 | Methylation | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine DNA_methylationmethylation of symmetrical ( CG and CNG ) sites was almost complete within the 5 ' Entityend of the nptII - transcribed region and the 35S promoter. |
| 0.9994 | Methylation | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine DNA_methylationmethylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed Entityregion and the 35S promoter. |
| 0.9990 | Methylation | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine DNA_methylationmethylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the 35S Entitypromoter . |
| 0.9980 | Methylation | After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine DNA_methylationmethylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the Entity35S promoter. |
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| 0.9999 | Methylation | Further, DNA_methylationmethylation of nonsymmetrical sites appeared de novo in the Entitypromoter , whereas this type of methylation was significantly reduced in the 3'end of the transcribed region when compared with locus 1. |
| 0.9981 | Methylation | Further, DNA_methylationmethylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the 3'end of the Entitytranscribed region when compared with locus 1. |
| 0.9993 | Methylation | Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of DNA_methylationmethylation was significantly reduced in the Entity3 ' end of the transcribed region when compared with locus 1. |
| 0.9987 | Methylation | Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of DNA_methylationmethylation was significantly reduced in the 3'end of the Entitytranscribed region when compared with locus 1. |
| 0.9978 | Methylation | Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of DNA_methylationmethylation was significantly reduced in the 3'end of the Entitytranscribed region when compared with locus 1. |
| 0.9967 | Methylation | Further, DNA_methylationmethylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the 3'end of the Entitytranscribed region when compared with locus 1. |
| 0.9966 | Methylation | Further, DNA_methylationmethylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the Entity3 ' end of the transcribed region when compared with locus 1. |
| 0.9929 | Methylation | Further, methylation of nonsymmetrical sites appeared de novo in the Entitypromoter , whereas this type of DNA_methylationmethylation was significantly reduced in the 3'end of the transcribed region when compared with locus 1. |
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| 0.9972 | Methylation | The protein and steady - state RNA levels remained low in locus 1E, whereas with nuclear run - on assays, no detectable amounts of primary transcripts were found along the nptII gene, indicating that the DNA_methylationmethylated Entitypromoter became inactivated. |
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| 0.9999 | Methylation | Frequent DNA_methylationmethylation of Proteinp16INK4A and p14ARF genes implicated in the evolution of chronic myeloid leukaemia from its chronic to accelerated phase. |
| 0.9999 | Methylation | Frequent DNA_methylationmethylation of p16INK4A and Proteinp14ARF genes implicated in the evolution of chronic myeloid leukaemia from its chronic to accelerated phase. |
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| 0.9958 | Methylation | Aberrant DNA_methylationmethylation of the p16 ( INK4A ) or p14 ( ARF ) Entitypromoters was found in 14 of 30 AP samples. |
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| 0.9996 | Methylation | The most common situation was the simultaneous DNA_methylationmethylation of both Entitypromoters . |
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| 0.9984 | Methylation | Our data indicate that p16 ( INK4A ) and p14 ( ARF ) are primary targets for inactivation by Entitypromoter DNA_methylationmethylation in the acceleration of CML. |
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| 1.0000 | Methylation | We also show that hSWI / SNF - associated PRMT5 can Methylationmethylate hypoacetylated Proteinhistones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.9999 | Methylation | We also show that hSWI / SNF - associated PRMT5 can Methylationmethylate hypoacetylated histones H3 and ProteinH4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.9989 | Methylation | We also show that hSWI / SNF - associated ProteinPRMT5 can Methylationmethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.9976 | Methylation | We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than Acetylationhyperacetylated histones H3 and ProteinH4 . |
| 0.9921 | Methylation | We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than Acetylationhyperacetylated Proteinhistones H3 and H4. |
| 0.9885 | Methylation | We also show that hSWI / SNF - associated PRMT5 can Methylationmethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and ProteinH4 . |
| 0.9769 | Methylation | We also show that hSWI / SNF - associated PRMT5 can Methylationmethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated Proteinhistones H3 and H4. |
| 0.9985 | Methylation | We also show that hSWI / SNF - associated PRMT5 can Acetylationmethylate hypoacetylated histones H3 and ProteinH4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.9921 | Methylation | We also show that hSWI / SNF - associated PRMT5 can Acetylationmethylate hypoacetylated Proteinhistones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.9894 | Methylation | We also show that hSWI / SNF - associated PRMT5 can methylate Acetylationhypoacetylated histones H3 and ProteinH4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.9736 | Methylation | We also show that hSWI / SNF - associated ProteinPRMT5 can Acetylationmethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.9462 | Methylation | We also show that hSWI / SNF - associated PRMT5 can methylate Acetylationhypoacetylated Proteinhistones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. |
| 0.5937 | Methylation | We also show that hSWI / SNF - associated PRMT5 can Acetylationmethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and ProteinH4 . |
| 0.4155 | Methylation | We also show that hSWI / SNF - associated PRMT5 can Acetylationmethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated Proteinhistones H3 and H4. |
| Methylation | We also show that hSWI / SNF - associated PRMT5 can methylate Deacetylationhypoacetylated histones H3 and ProteinH4 more efficiently than hyperacetylated histones H3 and H4. | |
| Methylation | We also show that hSWI / SNF - associated PRMT5 can methylate Deacetylationhypoacetylated Proteinhistones H3 and H4 more efficiently than hyperacetylated histones H3 and H4. | |
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| 0.9996 | Methylation | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by Acetylationhypoacetylation of Proteinhistones H3 and H4 and methylation of lysine 9 of histone H3 ( K9 - MeH3 ). |
| 0.9993 | Methylation | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and Methylationmethylation of Entitylysine 9 of histone H3 ( K9 - MeH3 ). |
| 0.9941 | Methylation | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by Acetylationhypoacetylation of histones H3 and ProteinH4 and methylation of lysine 9 of histone H3 ( K9 - MeH3 ). |
| 0.9978 | Methylation | BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and Methylationmethylation of Entitylysine 9 of histone H3 ( K9 - MeH3 ). |
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| 1.0000 | Methylation | Thermal stability and aggregation of sulfolobus solfataricus beta - glycosidase are dependent upon the MethylationN - epsilon - methylation of specific Entitylysyl residues : critical role of in vivo post - translational modifications. |
| 1.0000 | Methylation | Thermal stability and aggregation of sulfolobus solfataricus beta - glycosidase are dependent upon the MethylationN - epsilon - methylation of specific Entitylysyl residues : critical role of in vivo post - translational modifications. |
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| 0.9995 | Methylation | The aim of this work is to clarify some effects of methylation on the properties of Proteinbeta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, Methylationmethylated protein and its unmethylated counterpart, recombinantly expressed in Escherichia coli. |
| 0.9989 | Methylation | The aim of this work is to clarify some effects of methylation on the properties of Proteinbeta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, methylated protein and its Methylationunmethylated counterpart, recombinantly expressed in Escherichia coli. |
| 1.0000 | Methylation | The aim of this work is to clarify some effects of Methylationmethylation on the properties of Proteinbeta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, methylated protein and its unmethylated counterpart, recombinantly expressed in Escherichia coli. |
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| 1.0000 | Methylation | These observations suggest a role for the Methylationmethylation of Entitylysyl residues , located in selected domains, in the thermal stabilization of beta - glycosidase from S. solfataricus. |
| 0.9999 | Methylation | These observations suggest a role for the Methylationmethylation of Entitylysyl residues, located in selected domains, in the thermal stabilization of beta - glycosidase from S. solfataricus. |
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| 0.9956 | Methylation | The von Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of Hydroxylationhydroxylated Pro - 402 or EntityPro - 564 , both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ). |
| 0.9918 | Methylation | The von Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of Hydroxylationhydroxylated EntityPro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ). |
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| 0.9971 | Methylation | We show here that the role of Leu - 574 is to recruit ProteinPHD2 / HPH2 for Pro - 564 Hydroxylationhydroxylation . |
| 0.9956 | Methylation | We show here that the role of Leu - 574 is to recruit PHD2 / HPH2 for EntityPro - 564 Hydroxylationhydroxylation . |
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| 0.9957 | Methylation | An antibody specific for Hydroxylationhydroxylated EntityPro - 564 has been used to determine the hydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the hydroxylated HIF - 1alpha to the total amount. |
| 0.9937 | Methylation | An antibody specific for hydroxylated Pro - 564 has been used to determine the hydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the Hydroxylationhydroxylated ProteinHIF - 1alpha to the total amount. |
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| 0.9969 | Methylation | The nine - residue spacing between Pro - 564 and Leu - 574 is not obligatory for Entityprolyl Hydroxylationhydroxylation . |
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| 0.9978 | Methylation | CONCLUSION : The Proteintransferrin microheterogeneity pattern shifted towards reduced Glycosylationglycosylation and sialylation in addition to a decrease in total transferrin concentration in fetal blood compared to that of non - pregnant and pregnant women. |
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| 0.9993 | Methylation | Heterochromatin and Methylationtri - methylated Entitylysine 20 of histone H4 in animals. |
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| 0.9989 | Methylation | MethylationTri - methylated Entitylysine 20 on histone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells. |
| 0.9968 | Methylation | MethylationTri - methylated Entitylysine 20 on histone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells. |
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| 1.0000 | Methylation | To understand the interplay between various Proteinhistone modifications, including Acetylationacetylation and methylation, we performed a genome - wide chromatin structure analysis in a higher eukaryote. |
| 0.9990 | Methylation | To understand the interplay between various Proteinhistone modifications, including acetylation and Methylationmethylation , we performed a genome - wide chromatin structure analysis in a higher eukaryote. |
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| 1.0000 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being Acetylationhyperacetylated for ProteinH3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.9997 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and Methylationhypermethylated at EntityLys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.9991 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being Acetylationhyperacetylated for H3 and ProteinH4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.9828 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and Methylationhypermethylated at Lys 4 and EntityLys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.8726 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at EntityLys 4 and Lys 79 of H3, and inactive genes being Methylationhypomethylated and deacetylated at the same residues. |
| 0.8613 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and EntityLys 79 of H3, and inactive genes being Methylationhypomethylated and deacetylated at the same residues. |
| 0.7035 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and ProteinH4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and Deacetylationdeacetylated at the same residues. |
| 0.4697 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for ProteinH3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and Deacetylationdeacetylated at the same residues. |
| 0.9985 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and Methylationhypermethylated at EntityLys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.9500 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and Methylationhypermethylated at Lys 4 and EntityLys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues. |
| 0.6089 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and EntityLys 79 of H3, and inactive genes being Methylationhypomethylated and deacetylated at the same residues. |
| 0.5887 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at EntityLys 4 and Lys 79 of H3, and inactive genes being Methylationhypomethylated and deacetylated at the same residues. |
| 0.4885 | Methylation | We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and ProteinH4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being Methylationhypomethylated and deacetylated at the same residues. |
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| 0.9958 | Methylation | Less frequent Entitypromoter DNA_methylationhypermethylation of DLC - 1 gene in primary breast cancers. |
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| 0.9973 | Methylation | To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the DNA_methylationmethylation status of DLC - 1 Entitypromoter region in breast cancer cell lines and primary breast tumors. |
| 0.9950 | Methylation | To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the DNA_methylationmethylation status of DLC - 1 promoter Entityregion in breast cancer cell lines and primary breast tumors. |
| 0.9946 | Methylation | To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the DNA_methylationmethylation status of DLC - 1 Entitypromoter region in breast cancer cell lines and primary breast tumors. |
| 0.4963 | Methylation | To determine the implication of aberrant DNA_methylationmethylation , one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of DLC - 1 promoter Entityregion in breast cancer cell lines and primary breast tumors. |
| 0.4678 | Methylation | To determine the implication of aberrant DNA_methylationmethylation , one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of DLC - 1 Entitypromoter region in breast cancer cell lines and primary breast tumors. |
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| 0.9992 | Methylation | The gene silencing by methylation was also confirmed by the re - expression of DLC - 1 by the 5 - aza - 2'- deoxycytidine treatment in ProteinDLC - 1 DNA_methylationhypermethylated cell line. |
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| 0.9999 | Methylation | But the DNA_methylationmethylation of ProteinDLC - 1 gene was less frequently shown in primary breast cancers ( 10 % ). |
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| 0.9999 | Methylation | These data suggest that DNA_methylationhypermethylation is responsible for silencing of ProteinDLC - 1 gene in a limited portion of breast cancers. |
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| 1.0000 | Methylation | GlycosylationGlycosylation of the ProteinENV spike of primate immunodeficiency viruses and antibody neutralization. |
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| 0.9998 | Methylation | This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive Glycosylationglycosylation of the exposed regions of ProteinEnv within the trimer. |
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| 0.9985 | Methylation | Part of the strategy toward development of an optimally immunogenic Env spike will likely require modification of ProteinEnv Glycosylationglycosylation . |
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| 0.9994 | Methylation | The MSP assay detected DNA_methylationhypermethylation of p16 in 9 patients ( 22 % ), ProteinE - cadherin in 9 patients ( 22 % ), and RARbeta in 6 patients ( 15 % ). |
| 0.9993 | Methylation | The MSP assay detected DNA_methylationhypermethylation of Proteinp16 in 9 patients ( 22 % ), E - cadherin in 9 patients ( 22 % ), and RARbeta in 6 patients ( 15 % ). |
| 0.9988 | Methylation | The MSP assay detected DNA_methylationhypermethylation of p16 in 9 patients ( 22 % ), E - cadherin in 9 patients ( 22 % ), and ProteinRARbeta in 6 patients ( 15 % ). |
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| 0.9965 | Methylation | Human SWI / SNF - associated ProteinPRMT5 Methylationmethylates histone H3 arginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes. |
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| 0.9992 | Methylation | We have recently shown that PRMT5 can interact with flag - tagged BRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically Methylationmethylate histones H3 and ProteinH4 . |
| 0.9981 | Methylation | We have recently shown that PRMT5 can interact with flag - tagged BRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically Methylationmethylate Proteinhistones H3 and H4. |
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| 0.9996 | Methylation | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of Methylationmethylation by recombinant and hSWI / SNF - associated ProteinPRMT5 . |
| 0.9996 | Methylation | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 Entityarginine 3 are preferred sites of Methylationmethylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.9957 | Methylation | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 Entityarginine 8 and H4 arginine 3 are preferred sites of Methylationmethylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.9879 | Methylation | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 Entityarginine 8 and H4 arginine 3 are preferred sites of Methylationmethylation by recombinant and hSWI / SNF - associated PRMT5. |
| 0.5024 | Methylation | Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can Catalysismethylate H3 and H4 N - terminal tails, and show that H3 Entityarginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5. |
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| 1.0000 | Methylation | The hydrolysis and Glycosylationtransglycosylation properties of ProteinAmyM suggest that it has novel characteristics and can be regarded as an intermediate type of maltogenic amylase, alpha - amylase, and 4 - alpha - glucanotransferase. |
| 0.9714 | Methylation | The hydrolysis and Glycosylationtransglycosylation properties of AmyM suggest that it has novel characteristics and can be regarded as an intermediate type of maltogenic amylase, alpha - amylase, and Protein4 - alpha - glucanotransferase . |
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| 0.9995 | Methylation | Histone Methylationmethylation acts as an epigenetic regulator of chromatin activity through the modification of Entityarginine and lysine residues on histones H3 and H4. |
| 0.9981 | Methylation | Histone Methylationmethylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and Entitylysine residues on histones H3 and H4. |
| 0.9968 | Methylation | Histone Methylationmethylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and Entitylysine residues on histones H3 and H4. |
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| 1.0000 | Methylation | To examine the potential developmental roles of these modifications, we determined the global patterns of lysine Methylationmethylation involving EntityK9 on histone H3 and K20 on histone H4 in midgestation mouse embryos. |
| 0.9971 | Methylation | To examine the potential developmental roles of these modifications, we determined the global patterns of lysine Methylationmethylation involving K9 on histone H3 and EntityK20 on histone H4 in midgestation mouse embryos. |
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| 0.9970 | Methylation | Interestingly, three of these Methylationmodifications , histone H3 trimethyl EntityK9 , histone H4 monomethyl K20, and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium. |
| 0.9966 | Methylation | Interestingly, three of these Methylationmodifications , histone H3 trimethyl K9, histone H4 monomethyl EntityK20 , and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium. |
| 0.9941 | Methylation | Interestingly, three of these Methylationmodifications , histone H3 trimethyl K9, histone H4 monomethyl K20, and histone H4 trimethyl EntityK20 exhibited marked differences in their distribution within the neuroepithelium. |
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| 0.9991 | Methylation | Specifically, both histone H3 trimethyl K9 and H4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the EntityK9 Methylationmodification was limited to mitotic cells on the luminal surface. |
| 0.4343 | Methylation | Specifically, both histone H3 trimethyl K9 and H4 monomethyl EntityK20 were elevated in proliferating cells of the neural tube, which in the case of the K9 Methylationmodification was limited to mitotic cells on the luminal surface. |
| 0.4136 | Methylation | Specifically, both histone H3 trimethyl EntityK9 and H4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the K9 Methylationmodification was limited to mitotic cells on the luminal surface. |
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| 0.9962 | Methylation | The inverse relationship of histone H4 EntityK20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.9997 | Methylation | The inverse relationship of histone H4 EntityK20 Methylationmethyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the trimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.9964 | Methylation | The inverse relationship of histone H4 EntityK20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the trimethyl Methylationmodification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.9932 | Methylation | The inverse relationship of histone H4 EntityK20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.6355 | Methylation | The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl modification Methylationmodification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.5638 | Methylation | The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl modification Methylationmodification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.5345 | Methylation | The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl Methylationtrimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.5077 | Methylation | The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl Methylationmodification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.4898 | Methylation | The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl Methylationmodification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
| 0.4421 | Methylation | The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl modification Methylationtrimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells. |
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| 0.9982 | Methylation | Importantly, our results establish that histone Entitylysine Methylationmethylation occurs in a highly dynamic manner that is consistent with their function in an epigenetic program for cell division and differentiation. |
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| 0.9986 | Methylation | To investigate the effect of EGCG on H. pylori - induced toll - like receptor 4 ( TLR - 4 ) signaling, reverse transcription - polymerase chain reaction and Western blot analysis corresponding to Glycosylationglycosylated ProteinTLR - 4 were carried out. |
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| 0.9999 | Methylation | Helicobacter pylori infection stimulated the Glycosylationglycosylation of ProteinTLR - 4 , which initiates intracellular signaling in the infected host cell, but the pretreatment with EGCG completely blocked the TLR - 4 glycosylation. |
| 0.9993 | Methylation | Helicobacter pylori infection stimulated the glycosylation of TLR - 4, which initiates intracellular signaling in the infected host cell, but the pretreatment with EGCG completely blocked the ProteinTLR - 4 Glycosylationglycosylation . |
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| 0.9959 | Methylation | ProteinHistone H2B Ubiquitinationubiquitylation is associated with elongating RNA polymerase II. |
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| 0.9936 | Methylation | Rad6 - mediated Ubiquitinationubiquitylation of histone H2B at Entitylysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3. |
| 0.9927 | Methylation | Rad6 - mediated ubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of Entitylysine Methylationmethylation on histone H3. |
| 0.9764 | Methylation | Rad6 - mediated Ubiquitinationubiquitylation of histone H2B at Entitylysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3. |
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| 0.9985 | Methylation | However, how Rad6 and ProteinH2B Ubiquitinationubiquitylation contribute to the transcription and histone methylation processes is poorly understood. |
| 0.9977 | Methylation | However, how Rad6 and H2B ubiquitylation contribute to the transcription and Proteinhistone Methylationmethylation processes is poorly understood. |
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| 0.9945 | Methylation | This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes ProteinH2B Ubiquitinationubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes. |
| 0.7104 | Methylation | This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes ProteinH2B Ubiquitinationubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes. |
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| 0.9863 | Methylation | In support of a role for Rad6 - dependent ProteinH2B Ubiquitinationubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation. |
| 0.7766 | Methylation | In support of a role for ProteinRad6 - dependent H2B Ubiquitinationubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation. |
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| 0.9990 | Methylation | Finally, we show that Saccharomyces cerevisiae mutants bearing defects in the pathway to ProteinH2B Ubiquitinationubiquitylation display transcription elongation defects as assayed by 6 - azauracil sensitivity. |
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| 0.9982 | Methylation | Collectively, our results indicate a role for Rad6 and ProteinH2B Ubiquitinationubiquitylation during the elongation cycle of transcription and suggest a mechanism by which H3 methylation may be regulated. |
| 0.9982 | Methylation | Collectively, our results indicate a role for Rad6 and H2B ubiquitylation during the elongation cycle of transcription and suggest a mechanism by which ProteinH3 Methylationmethylation may be regulated. |
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